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Objectives: An objective categorization of respiratory infections based on outcomes is an unmet clinical need. Ventilator-associated pneumonia and tracheobronchitis remain used in clinical practice, whereas ventilator-associated events (VAE) are limited to surveillance purposes., Research Methodology/design: This was a secondary analysis from a multicentre observational prospective cohort study. VAE were defined as a sustained increase in minimum Oxygen inspired fraction (FiO2) and/or Positive end-expiratory pressures (PEEP) of ≥ 0.2/2 cm H 2 O respectively, or an increase of 0.15 FiO 2  + 1 cm H20 positive end-expiratory pressures for ≥ 1 calendar-day., Setting: 15 Paediatric Intensive Care Units., Main Outcome Measures: Mechanical ventilation duration, intensive care and hospital length of stay; (LOS) and mortality., Results: A cohort of 391 ventilated children with an age (median, [Interquartile Ranges]) of 1 year[0.2-5.3] and 7 days[5-10] of mechanical ventilation were included. Intensive care and hospital stays were 11 [7-19] and 21 [14-39] days, respectively. Mortality was 5.9 %. Fifty-eight ventilator-associated respiratory infections were documented among 57 patients: Seventeen (29.3 %) qualified as ventilator-associated pneumonia (VAP) and 41 (70.7 %) as ventilator-associated tracheobronchitis (VAT). Eight pneumonias and 16 tracheobronchitis (47 % vs 39 %,P = 0.571) required positive end-expiratory pressure or oxygen increases consistent with ventilator-associated criteria. Pneumonias did not significantly impact on outcomes when compared to tracheobronchitis. In contrast, infections (pneumonia or tracheobronchitis) following VAEs criteria were associated with > 6, 8 and 15 extra-days of ventilation (16 vs 9.5, P = 0.001), intensive care stay (23.5 vs 15; P = 0.004) and hospital stay (39 vs 24; P = 0.015), respectively., Conclusion: When assessing ventilated children with respiratory infections, VAE apparently is associated with higher ventilator-dependency and LOS compared with pneumonia or tracheobronchitis., Implications for Practice: Incorporating the modification of ventilatory settings for further categorization of the respiratory infections may facilitate therapeutic management among ventilated patients., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Pulmonary extra-intestinal manifestations of inflammatory bowel disease are rare, comprising 0.21% to 0.4% of the inflammatory bowel disease population. Common symptoms include cough, chest pain, and dyspnea. Abnormal pulmonary function tests are common in these patients, with restrictive, obstructive, and diffusion capacity defects. CT scanning remains the most sensitive imaging technique to detect abnormalities. Pulmonary manifestations are diverse and include airway, parenchymal, and pleural disease. Large airway disease predominates, particularly bronchiectasis. Upper airway disease is rare but concerning for the development of acute airway compromise. To our knowledge, there are no reports of concurrent mediastinitis with tracheitis in the setting of inflammatory bowel disease. We present a case of a patient with ulcerative proctitis who experienced the development of inflammatory tracheitis and mediastinitis. Her disease responded to systemic steroids and biologic therapy. In addition to our case, we reviewed the literature and provide an approach to pulmonary complications as extra-intestinal manifestation of inflammatory bowel disease., (Copyright © 2021 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Pulmonary manifestations of inflammatory bowel disease are increasingly recognized in patients with ulcerative colitis and Crohn's disease. Most commonly, incidental abnormalities are noted on chest imaging or pulmonary function tests. Although clinically significant pulmonary disease is less common, it can carry significant morbidity for patients. We review the presenting symptoms, workup, and management for several of the more common forms of inflammatory bowel disease-related pulmonary disease. Increased awareness of the spectrum of extraintestinal inflammatory bowel disease will help providers more readily recognize this phenomenon in their own patients and more comprehensively address the protean sequelae of inflammatory bowel disease., (Copyright © 2019 Elsevier Inc. All rights reserved.)

A 19 year female, presented with life threatening haemoptysis and cough with minimum expectoration for 3 months. Bronchoscopy showed multiple nodules in airway. The direct microscopy and culture of sputum revealed fungal elements and Aspergillus flavus respectively. Serum Galactomannan was positive. Thus diagnosis of invasive aspergillus tracheo-bronchitis made. She responded to voriconazole. Aspergillus tracheo-bronchitis is a rare form of invasive pulmonary aspergillosis in immuno-competent host. Aspergillus spp in respiratory samples should not be routinely discarded as colonization., (© Journal of the Association of Physicians of India 2011.)

The aim of the present study was to analyze clinical and cytokine features of recurrent respiratory system diseases in children with toxocariasis. 50 children aged 1 to 17 years (mean age - 10±5 years) with recurrent current of respiratory system disorders were studied. During the survey such clinical manifestations of the respiratory system disorders as obstructive bronchitis (50%), bronchial asthma (30%), pneumonia (10%) and laryngotracheitis (10%) have been revealed. Statistical analysis of the results was performed using the software package STATISTICA 6.1 (SNANSOFT). We have shown that the disorders of respiratory system in case of toxocariasis invasion often occur with severe intoxication and bronchial obstruction syndromes, temperature reaction, respiratory insufficiency and hepatomegaly. A prolonged course of the disease has been noted. "Inflammatory" indicators of general blood analysis, such as leukocytosis and increased of ESR have been recorded in patients with respiratory system disorders in children with T.canis infection significantly more often, significant "allergic" laboratory changes were in the form of eosinophilia. High average levels of pro-inflammatory IL-6, as well as low levels of IL 5 have been determined in children suffering from the respiratory system disorders and with toxocariasis invasion in the anamnesis. The obtained findings require further study.

It was analyzed the incidences of laryngotracheitis (LT) in children aged 0 to 14 years in Vinnytsya between 1995 and 2008. It was studied seasonal and circadian rhythms of LT in children. The seasonal variations of LT are characterized by two-wave curve with peaks in October and March, and with a significant decrease in July and August. The incidences of LT in October and March exceed the incidences of LT in July and August in 2.6 times. Circadian variation of LT is characterized by peak at night. The incidences of LT at night exceed the incidences in the morning in 2.6 times. The total number of the incidences of LT in the evening and at night exceed the total number of the incidences of LT in the morning and in the afternoon in 1.7 times. The maximum of incidences of LT to minimum of incidences of LT per hour ratio is 5:1 in girls compared to 4:1 in boys.

Purpose of Review: To evaluate the data on antimicrobial therapy for ventilator-associated tracheobronchitis (VAT) to prevent ventilator-associated pneumonia (VAP), and its impact on patient outcomes., Recent Findings: Mechanically ventilated patients are at increased risk for tracheal colonization with bacterial pathogens that may progress to VAT and/or VAP. Previous studies suggest that 10-30% of patients with VAT progress to VAP, which results in increased morbidity but not mortality. Several natural history studies and small randomized controlled trials and a meta-analysis reported that appropriate, pre-emptive antibiotic treatment for VAT reduces VAP, duration of intubation and length of ICU stay., Summary: This review focuses on diagnostic criteria for VAT and VAP, etiologic agents, rationale and benefits of initiating pre-emptive, appropriate antibiotic treatment for VAT to prevent VAP, improve patient outcomes and associated acute and chronic healthcare costs.

We present the case of a 54-year-old male, who presented with respiratory complaints four months after he underwent renal transplantation. Bronchoscopy showed ulcerated mucosa of the left main bronchus and computed tomography (CT) of the thorax showed foci of air within the bronchial wall. A biopsy from the lesion showed septate fungal hyphae, dichotomously branching at acute angles. A locally invasive Aspergillus ulcerative tracheobronchitis with no parenchymal involvement is an important cause of tracheobronchitis in post-renal transplant patients. An early diagnosis and institution of appropriate treatment can improve the outcome. A combination treatment of caspofungin and voriconazole can be considered if patient is not responding to voriconazole alone.

Background: With the acceleration of industrialization in low or middle-income nations, the prevalence of respiratory symptoms among older adults is even more significant now in China. Contemporary treatments using Western medicine, such as anti-inflammatory regimens, may be effective in relieving the symptoms, but may have unexpected side effects. Some natural products may be effective in improving respiratory functions, yet their efficacies remain to be examined in randomized, placebo-controlled studies. To evaluate the effects of Lung Support Formula, a nutritional supplement which contains naturally derived Chinese herbal medicines, we conducted a clinical study among older adults in Shanghai, China., Methods: A total of 100 patients over 50 years old were recruited and blindly randomized into the treatment or control group. The subjects took either 1 Lung Support Formula capsule or a placebo capsule twice a day for 12 weeks. All subjects were followed-up every 4 weeks to perform investigative and clinical examinations. Repeated measure of analysis of variance was employed to compare the trend of respiratory symptoms scores between the 2 groups during 12 weeks of follow-up., Results: Fifty patients from the treatment group and 49 patients in the control group completed the 3-month follow-up. No adverse events were reported in the treatment duration. The percentage of patients reported to have chronic cough, chronic expectoration and chronic bronchitis were significantly decreased in the treatment group when compared with baseline after a 3-month intervention (P < 0.05). The respiratory symptoms scores declined gradually with the lapse of time (P < 0.05) in the treatment group and there were no significant changes in the control group by repeated measure of analysis of variance (P > 0.05)., Conclusions: The clinical research shows that use of Lung Support Formula shows significant improvements of respiratory symptoms and is well-tolerated in short-term use among older adults. An additional study involving more subjects and longer-term follow-up would be needed to provide convincing evidence of the improvement of respiratory symptoms in the treatment group.

Asthma is a chronic condition with unknown pathogenesis, and recent evidence suggests that enhanced airway epithelial chloride (Cl-) secretion plays a role in the disease. However, the molecular mechanism underlying Cl- secretion and its relevance in asthma pathophysiology remain unknown. To determine the role of the solute carrier family 26, member 9 (SLC26A9) Cl- channel in asthma, we induced Th2-mediated inflammation via IL-13 treatment in wild-type and Slc26a9-deficient mice and compared the effects on airway ion transport, morphology, and mucus content. We found that IL-13 treatment increased Cl- secretion in the airways of wild-type but not Slc26a9-deficient mice. While IL-13-induced mucus overproduction was similar in both strains, treated Slc26a9-deficient mice exhibited airway mucus obstruction, which did not occur in wild-type controls. In a study involving healthy children and asthmatics, a polymorphism in the 3' UTR of SLC26A9 that reduced protein expression in vitro was associated with asthma. Our data demonstrate that the SLC26A9 Cl- channel is activated in airway inflammation and suggest that SLC26A9-mediated Cl- secretion is essential for preventing airway obstruction in allergic airway disease. These results indicate that SLC26A9 may serve as a therapeutic target for airway diseases associated with mucus plugging.

Protease-activated receptor 2 (PAR-2) is a G protein-coupled receptor possibly involved in the pathogenesis of asthma. PAR-2 also modulates ion transport in cultured epithelial cells, but these effects in native airways are controversial. The influence of allergic inflammation on PAR-2-induced changes in ion transport has received little attention. Here, we studied immediate changes in transepithelial short circuit current (I (sc)) induced by PAR-2 activation in the tracheas of naive and allergic mice. Activation of PAR-2 with an apically added activation peptide (AP) induced a small increase in I (sc), while a much larger increase was observed following basolateral AP addition. In ovalbumin-sensitized and -challenged animals used as a model of allergic airway inflammation, the effect of basolateral AP addition was enhanced. Responses to basolateral AP in both naive and allergic mice were not decreased by blocking sodium absorption with amiloride or CFTR function with CFTR(inh)172 but were reduced by the cyclooxygenase inhibitor indomethacin and largely blocked (>80%) by niflumic acid, a calcium-activated chloride channels' (CaCC) blocker. Allergic mice also showed an enhanced response to ATP and thapsigargin. There was no change in mRNA expression of Par-2 or of the chloride channels Ano1 (Tmem16a) and Bestrophin 2 in tracheas from allergic mice, while mRNA levels of Bestrophin 1 were increased. In conclusion, basolateral PAR-2 activation in the mouse airways led to increased anion secretion through apical CaCC, which was more pronounced in allergic animals. This could be a protective mechanism aimed at clearing allergens and defending against mucus plugging.

Objectives: The purpose of this study was to develop an animal model for the study of mucus overproduction and to assess the effect of a 14-membered macrolide antibiotic and a glucocorticoid on lipopolysaccharide (LPS)-induced mucus production., Methods: Tracheas from donor rats were homografted to recipient rats for 4 weeks, and the usefulness of this tracheal homograft model in the study of mucus production was examined., Results: Oral administration of clarithromycin (CAM) to recipient rats for 4 weeks significantly reduced LPS-induced mucus production in the homografted trachea. Dexamethasone administered for 4 weeks also significantly reduced the mucus volume in LPS-treated homografted trachea compared with that in the control rats. The implanted trachea containing control medium was not histologically different from normal trachea. When the medium instilled into the implanted trachea contained 1 μg/ml LPS, the volume and spinability of mucus produced in the tracheal lumen were significantly increased compared to those in the trachea instilled with control medium. Goblet cell metaplasia was also observed in the implanted trachea containing LPS., Conclusions: The present study shows that LPS-administered homografted trachea is a good animal model of chronic hypersecretory diseases of the upper and lower airways. CAM and dexamethasone could be treatment choices in such hypersecretory diseases., (Copyright © 2011 S. Karger AG, Basel.)

Objective: To describe the clinical manifestations of parainfluenza virus (PIV) infection and to characterize biochemical markers of PIV disease severity., Patients and Methods: We reviewed the medical records of 165 children who had a nasal wash culture positive for PIV at our institution between 1998 and 2008. Nasal wash samples were assayed for 26 inflammatory mediators using Luminex bead proteomics., Results: A total of 153 patients, ages 2 weeks to 12 years, with single virus infection were included in our final analysis. Fifty-two patients were infected with PIV1, 19 with PIV2, 74 with PIV3, and 8 with PIV4. Lower respiratory tract infection (LRTI) was diagnosed in 67 (44%) patients, 21 (14%) had laryngotracheobronchitis, and 49 (32%) had an upper respiratory infection other than laryngotracheobronchitis. LRTI was diagnosed in 54% of patients infected with PIV3, 35% of those infected with PIV1, 26% of those with PIV2, and 50% of those with PIV4. Compared with uninfected control patients, PIV-infected patients had higher nasal wash concentrations of interleukin-6, CX-chemokine ligand 8 (CXCL8 or interleukin-8), CCL3 (macrophage inflammatory protein-1alpha), CCL4 (macrophage inflammatory protein-1beta), CXCL9 (monokine induced by interferon gamma), and CCL5 (regulated upon activation, normal T cell expressed and secreted (RANTES). Patients with LRTI, moderate or severe illness, and PIV 1 or 3 (respirovirus) infection had higher nasal wash concentrations of CXCL8 when compared with patients with upper respiratory infection, mild illness, or PIV 2 and 4 (rubulavirus) infection (P < 0.05)., Conclusions: PIV infection causes a spectrum of illnesses associated with the expression and release of several proinflammatory mediators. Of note, elevated concentrations of CXCL8 in nasal wash samples are associated with more severe forms of PIV disease.

Background: Bacterial tracheitis may cause life-threatening airway obstruction., Methods: Records of patients admitted to the pediatric wards of Mackay Memorial Hospital between 1994 and 2005 with a diagnosis of bacterial tracheitis made on bronchoscopic visualization of thick membranous tracheal secretions were retrospectively reviewed., Results: A total of 40 patients (aged 1 month-8 years, 29 [73%] under 3 years old) were included. Cough, fever, dyspnea, and hoarseness were the commonest symptoms. Fourteen patients (21%) required intubation. The most frequently isolated bacteriae were alpha-hemolytic streptococcus (in 11, 38%), pseudomonas (5, 17%), and Staphylococcus aureus (4, 14%). Intubation was more frequent in patients seen between 1994 and 1999 compared with those seen later (8/12 early vs 9/28 late). In the early period alpha-hemolytic streptococcus (55%) and pseudomonas (36%) were isolated. In the later period the most frequently isolated bacteria was alpha-hemolytic streptococcus (28%), followed by S. aureus (22%). No patients died, but those with pseudomonas infection had more severe complications, including tracheal stenosis. The average hospital stay in the early period was 26.2 +/- 20.5 days versus 9.1 +/- 4.8 days in the late period. The corresponding lengths of stay in the intensive care unit were 10.5 +/- 11.5 days and 2.0 +/- 2.2 days., Conclusions: Bacterial tracheitis requiring hospitalization of children appeared to be milder in the second half of the study period. Pseudomonas tracheitis tends to have a severe course.

A child presented with features of bacterial tracheitis with complete response to therapy. He presented with a recurrence one week later. A foreign body in the tracheal wall was diagnosed and removed by bronchoscopy. Tracheal intubation for airway management and tracheal toileting are not enough in bacterial tracheitis; bronchoscopy should be considered to diagnose any underlying cause.

Staged development of dysbiotic disturbance of the upper airways was revealed in children suffering from stenosing laryngotracheitis in the presence of viral infection. Chronic persistent virus-bacterial inflammation of respiratory tract mucosa and resultant hypersensitivity of the airways produce chronic defects in lung ventilation in patients with recurrent stenosing laryngotracheitis. High sensitivity of the airways to histamine is related to bioelectric activity of the brain characterized by dominant irritation of the mesencephalo-diencephalic structures. Typical features of the curve flow-volume and paradoxic result of the test with broncholytic drugs verified tracheobronchial dyskinesia in patients with stenosing laryngotracheitis. Such dyskinesia promoted the recurrent disease with transformation into bronchial asthma.

Background: Acupuncture therapy for obstructive respiratory diseases has been effectively used in clinical practice and the acupuncture points or acupoints of Zhongfu and Tiantu are commonly-used acupoints to treat patients with the diseases. Since the impaired mucociliary clearance is among the most important features of airway inflammation in most obstructive respiratory diseases, the effect of needle puncture and electro-acupuncture at the specific acupoints on tracheal mucociliary clearance was investigated in anesthetized quails., Methods: Mucociliary transport velocity on tracheal mucosa was measured through observing the optimal pathway, and fucose and protein contents in tracheal lavages were determined with biochemical methods. In the therapeutic group, needle puncture or electro-acupuncture stimulation to the acupoints was applied without or with constant current output in 2 mA and at frequency of 100 Hz for 60 minutes. In the sham group, electro-acupuncture stimulation to Liangmen was applied., Results: Our present experiments demonstrated that the electro-acupuncture stimulation to Zhongfu and Tiantu significantly increased tracheal mucociliary transport velocity and decreased the content of protein in the tracheal lavage, compared with the control group. Moreover, either needle puncture or electro-acupuncture stimulation to Zhongfu and Tiantu significantly reverted the human neutrophil elastase-induced decrease in tracheal mucociliary transport velocity and human neutrophil elastase -induced increase in the contents of fucose and protein in the tracheal lavage, compared with the control group., Conclusion: These results suggest that either needle puncture or electro-acupuncture stimulation to the effective acupoints significantly improves both airway mucociliary clearance and the airway surface liquid and that the improvements maybe ascribed to both the special function of the points and the substantial stimulation of electricity.

Respiratory epithelial cells play a crucial role in the inflammatory response in endotoxin-induced lung injury, an experimental model for acute lung injury. To determine the role of epithelial cells in the upper respiratory compartment in the inflammatory response to endotoxin, we exposed tracheobronchial epithelial cells (TBEC) to lipopolysaccharide (LPS). Expression of inflammatory mediators was analyzed, and the biological implications were assessed using chemotaxis and adherence assays. Epithelial cell necrosis and apoptosis were determined to identify LPS-induced cell damage. Treatment of TBEC with LPS induced enhanced protein expression of cytokines and chemokines (increases of 235-654%, P < 0.05), with increased chemotactic activity regarding neutrophil recruitment. Expression of the intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was enhanced by 52-101% (P < 0.0001). This upregulation led to increased adhesion of neutrophils, with >95% adherence to TBEC after LPS stimulation, which could be blocked by either ICAM-1 (69%) or VCAM-1 antibodies (55%) (P < 0.05). Enhanced neutrophil-induced necrosis of TBEC was observed when TBEC were exposed to LPS. Reduced neutrophil adherence by ICAM-1 or VCAM-1 antibodies resulted in significantly lower TBEC death (52 and 34%, respectively, P < 0.05). Therefore, tight adherence of neutrophils to TBEC appears to promote epithelial cell killing. In addition to indirect effector cell-induced TBEC death, direct LPS-induced cell damage was seen with increased apoptosis rate in LPS-stimulated TBEC (36% increase of caspase-3, P < 0.01). These data provide evidence that LPS induces TBEC killing in a necrosis- and apoptosis-dependent manner.

Study Objectives: Unopposed activity of the serine protease, human leukocyte elastase (HLE), is detectable in the airways of patients with purulent tracheobronchitis. The aim of this study was to assess the compartmentalization of HLE activity in the liquid sol phase and the solid gel phase of airway secretions., Design: Seventy samples of tracheobrochial aspirates were obtained from patients who had hypersecretion and were receiving mechanical ventilation., Methods: Samples were separated into sol and gel ("mucous pellet") phases, and HLE activity was measured using chromogenic substrate degradation. HLE was eluted from the mucous pellet using hypertonic saline solution, 1 mol/L, or bovine pancreatic deoxyribonuclease (DNase), 16 micromol/L., Results: HLE activity partitioned between the sol and gel phases of the secretions, with most of the activity present in the gel phase (32:1 ratio of gel to sol HLE activity). The activity of HLE was 95% inhibited when bound to the gel phase, but activity appeared to be largely restored after elution from the gel phase. The gel phase was capable of binding additional exogenous HLE, and its binding capacity for exogenous HLE was not saturated by concentrations that exceeded the highest clinically relevant HLE levels (1.1 mg/mL). Hypertonic saline solution and DNase I efficiently liberated endogenous and exogenous gel phase-bound HLE activity, suggesting that electrostatic bonds and DNA, respectively, play important roles in binding HLE to the gel phase., Conclusions: The solid phase of airway secretions is a more important modulator of elastase-antielastase balance than has been previously recognized.

Objective: Bacterial tracheitis (BT) is a condition that can cause fatal airway obstruction. We evaluated our experience with BT over a 10-year period., Study Design: Retrospective review of patients treated for BT between 1991 and 2001., Results: Ninety-four cases were evaluated. The mean patient age was 7.9 years. At presentation, 60% were afebrile, and the mean WBC count was 10.8 x 10(3)/mm3 . Only 53% of patients required intubation. Younger children were more likely to require this intervention. S. aureus was the most commonly cultured bacteria, while isolation of M. catarrhalis was associated with a higher intubation rate. A pathologic virus was isolated in 64% of the 34 cultures performed. Only 9 patients were described as "toxic," and 6 presented in respiratory extremis. There were no deaths., Conclusion and Significance: A subset of patients with tracheal membranes has a less severe clinical appearance. Nonetheless, these patients require debridement and aggressive medical treatment. We propose that the term "exudative tracheitis" (ET) better describes this entity. Older patients who are less systemically ill and rapidly respond to local and systemic therapy are characteristic of ET., Ebm Rating: C.

Objective: To examine the potential of the two tumour necrosis factor (TNF) inhibitors infliximab and etanercept as remission-inducing agents in chronic therapy-resistant inflammatory disorders of immune or non-immune pathogenesis., Methods: 14 patients with adult Still's disease/macrophage activation syndrome (4), Wegener's disease (3), Behçet's disease (3), keratoscleritis (1), lymphomatous tracheo-bronchitis (1) Cogan's syndrome (1), and rapidly destructive crystal arthropathy (1) were treated with infliximab (n = 10) and etanercept (n = 4). All patients showed organ-threatening progression of their diseases with resistance to conventional immunosuppressive medication. Therapeutic benefit was assessed clinically and by documenting organ-specific functional and morphological alterations. Side effects were compared with the data of our clinic's rheumatoid arthritis (RA) patients treated by TNF inhibitors., Results: A rapid and dramatic beneficial effect was documented in 9 patients and a moderate one in 5. Best responses (clinical and laboratory parameters) were seen in patients with macrophage activation syndrome/adult Still's disease and Behçet's disease, while the results were less impressive in those with Wegener's disease, Cogan's syndrome, idiopathic cerato-scleritis and lymphomatous tracheobronchitis. In all cases immunosuppressive agents and systemic glucocorticoids could be reduced or discontinued., Conclusions: TNF inhibition may be highly effective in patients with severe, therapy-resistant chronic inflammatory disorders.

We report the case of a young woman with Crohn's disease of the bowel who presented with a purulent tracheobronchitis and life-threatening upper airway obstruction. Fibreoptic bronchoscopy demonstrated severe tracheal and upper bronchial pseudotumours and stenosis. The role of recent discontinuation of corticosteroids, for quiescent inflammatory bowel disease, in the development of endobronchial disease and the dramatic response in airway patency after reintroduction of prednisolone in this rare complication of Crohn's disease are discussed.

The present study aims to investigate the neurophysiological effects of recurrent laryngeal nerve and thoracic vagus nerve on the non-cholinergic regulation of neurogenic plasma extravasation of the rat trachea, bronchi, and esophagus. Through thoracotomy, three nerve components, the right thoracic vagal trunk, thoracic vagus nerve, and recurrent laryngeal nerve, were identified. The experiment was sequentially conducted in four steps. First, the individual nerve component was electrically stimulated and the induced inflammatory responses, as quantified by the area density of India ink-labelled blood vessels in the trachea, bronchial trees and esophagus, were compared. Second, we assessed the relative importance of medial and lateral side of the right thoracic vagus nerve in inducing the inflammatory responses by alternative stimulation of one side with simultaneous severance of the other side of this nerve. Third, we examined the effects of transection of the lateral half of the right thoracic vagus nerve on the degeneration of axon fibers located at the following three sites: the nerve segment proximal to cutting site, bronchial and esophageal nerve branches. Finally, we directly observed the inflammatory histopathology of the right lower trachea after stimulation of the medial half of the right thoracic vagus nerve with transection of its lateral half. In this study, we found that the right recurrent laryngeal nerve was predominant in mediating the neurogenic inflammatory responses of upper and dorsal portions of trachea, whereas the right thoracic vagus nerve was predominant in mediating those of the right lower ventral wall of trachea, right main bronchus, and right lobar bronchial trees. The axon fibers of the right thoracic vagus nerve responsible for mediating the neurogenic inflammatory responses of the right lower ventral trachea were mainly accumulated in the medial half, whereas those innervating the right main bronchus, right lobar bronchial trees, and lower esophagus were largely in the lateral half of this nerve. Transection of the lateral half of the right thoracic vagus nerve resulted in significant degeneration of myelinated fibers in its bronchial and esophageal nerve branches. Histopathological examination of the right lower trachea after electrical stimulation of the medial half of thoracic vagus nerve demonstrated the silver-stained leaky venules with accumulations of inflammatory cells. We thus concluded that afferent C-fibers to upper and dorsal portions of trachea were mainly from recurrent laryngeal nerve. In contrast, the neurogenic inflammatory responses of the right lower trachea were predominantly mediated by the medial half of the right thoracic vagus nerve, and those of the right main bronchus, bronchial trees and lower esophagus were largely by the lateral half of this nerve.

The majority of airway sensory innervation originates from afferent neurons whose somata reside in vagal (nodose and jugular) ganglia. Using guinea pigs immunized with chick ovalbumin, we have discovered that airway inflammation provokes phenotypic changes in the tachykinin responsiveness of nodose neurons. Bath application of substance P (SP; 0.1 to 10 microM) to nodose neurons isolated from guinea pigs with normal uninflamed airways did not elicit measurable changes in resting electrophysiological properties. In sharp contrast, 80% of nodose neurons isolated 24 h after in vivo aerosolized antigen challenge of the airway were depolarized by 100 nM SP. Inhalation of a nonantigenic protein did not evoke the expression of SP responses. Pharmacological analysis revealed that SP responses unmasked by airway inflammation were mediated by neurokinin-2 (NK-2) tachykinin receptors. There are several potential mechanisms for transduction of an "unmasking signal" from the inflamed airway to vagal afferent somata. The vagus nerve may relay the signal, either through anterograde transport and/or nerve impulse activity. Alternatively, a signal generated by airway inflammation may be carried by the circulation to the nodose ganglia. Unilateral vagotomy significantly reduced the percentage of SP-responsive neurons compared with intact controls, suggesting that the vagus nerve is required for unmasking of NK-2 responses.

Background: We have shown that some patients presenting with chronic bronchodilator-resistant non-productive cough have global atopic tendency and airway cough hypersensitivity without non-specific bronchial hyperresponsiveness, abbreviated as atopic cough. The cough is successfully treated with histamine H1-antagonists and/or glucocorticoids., Objective: This prospective study was conducted to elucidate the histological feature of atopic cough., Methods: Tracheal and bronchial mucosa obtained by transbronchoscopic biopsy and bronchoalveolar lavage (BAL) cell component were studied with special emphasis on eosinophils in eight non-smokers diagnosed with atopic cough, all of whom had increased sensitivity of cough response to inhaled capsaicin, normal lung function and bronchial responsiveness to methacholine and normal chest roentgenogram. Their cough completely resolved on histamine H1-antagonists and/or glucocorticoids. Transbronchoscopic tracheal and bronchial biopsy and BAL were also performed in healthy non-smokers as a control., Results: A small number of eosinophils was detected in subepithelium of trachea in six of seven patients and in subepithelium of bronchi in seven of eight cough patients. The numbers of eosinophils in subepithelium of trachea and bronchi were significantly increased in the patients compared with control subjects. There was no BAL eosinophilia in any patients., Conclusion: It is concluded that eosinophilic tracheobronchitis and cough hypersensitivity are pathological and physiological characteristics of atopic cough.

Airway inflammation is a prominent feature of chronic obstructive diseases of the airways, including asthma, bronchiectasis, chronic bronchitis, and diffuse panbronchiolitis. Neutrophils are implicated in the pathogenesis of these diseases. The present review discusses the role of interleukin-8 (IL-8), a neutrophil chemo-attractant, in neutrophil accumulation in the airways, and the mechanisms of inducing IL-8 expression. IL-8 presents in the sputum of patients with inflammatory airway diseases, and accounts in large part for the chemo-attractant activity present. Focusing on Pseudomonas aeruginosa as the stimulus, it was discovered that when a supernatant of bacterial culture is introduced into the airways in vivo, bacterial products induce IL-8 expression in surface airway epithelial cells and the recruitment of neutrophils into the airways. The neutrophil chemotactic activity of the airway fluid was inhibited by an IL-8 antibody. The luminal IL-8 concentration increased in response to instillation of bacteria, and an inhibitor of neutrophil recruitment markedly reduced the IL-8 levels. From these results, it was speculated that bacteria-induced neutrophil accumulation in the airways involves a cascade of events, and that early neutrophil recruitment in response to bacteria is due to epithelium-derived IL-8, while the amplification of the response is due, at least in part, to IL-8 induction in the neutrophils themselves.

Angiogenesis is a feature of chronic inflammation produced by Mycoplasma pulmonis infection of the respiratory tract. The mechanism of this angiogenesis is unknown, but cellular growth factors and matrix remodeling proteases produced by inflammatory cells are likely to be involved. The goal of this study was to determine the relationship between changes in the number, shape, and distribution of ED2-immunoreactive macrophages and the development of angiogenesis in the tracheal mucosa of Wistar rats after M. pulmonis infection. In pathogen-free rats, ED2-positive cells were scattered in the airway mucosa (261 +/- 42 cells/mm2 of surface, mean +/- SE). Most cells were irregularly shaped and had moderate ED2 immunoreactivity. No lymphoid tissue was present. The number of ED2-positive cells increased rapidly after infection, was 120% above baseline at 1 wk, and remained significantly increased throughout the 4-wk study (P < 0.05). Angiogenesis was first detected at 2 wk, and at 3 wk the vessel length density was nearly 8-fold the pathogen-free value. At 3 and 4 wk, focal sites of angiogenesis coincided with discrete clusters of round, strongly immunoreactive ED2-positive cells (1,340 +/- 124 cells/mm2) in polyp-like collections of mucosal lymphoid tissue. The close association of distinctive ED2-positive cells with angiogenic blood vessels suggests a relationship between a subset of tissue macrophages and the angiogenesis associated with M. pulmonis infection. The time course of the changes indicates that the initial influx of ED2-positive macrophages precedes the angiogenesis, and the rounding of the cells parallels the growth of new vessels.

Bacterial tracheitis is characterized by acute upper-airway obstruction and purulent secretions within the trachea. Historically, affected children were young, stridorous, and toxic-appearing and required tracheal intubation, and morbidity and mortality were significant. Staphylococcus aureus was the most common organism involved. During the 14 months of this retrospective study, 46 children were admitted to the pediatric intensive care unit because of this diagnosis, and their medical records were reviewed. Compared with those in previous reports, children in this study were older (mean +/- standard error of the mean [SEM], 69.3 +/- 6.8 months) and less toxic. Only 26 (57%) of 46 patients required tracheal intubation. Intubated patients were significantly younger than nonintubated patients (mean +/- SEM, 46.9 +/- 6.5 vs. 98.9 +/- 9.9 months). Moraxella catarrhalis was identified in 12 (27%) of 45 bacterial respiratory cultures, while influenza A virus was recovered from 18 (72%) of 25 viral respiratory cultures. There were no major complications. This series represents the largest reported cohort of patients with this condition and suggests an epidemiological change toward a less morbid condition.

Gicerin is a novel cell adhesion protein that belongs to the immunoglobulin superfamily. Gicerin protein adheres to neurite outgrowth factor, an extracellular matrix protein in the laminin family, and also exhibits homophilic adhesion. In the present study, we investigated the involvement of gicerin and neurite outgrowth factor in tracheal development and regeneration. In an early embryonic stage, gicerin protein was highly expressed in tracheal epithelial cells, but not in loosely arranged mesenchymal cells. During development, mesenchymal cells become condensed around the tracheal epithelium and then differentiate into muscle and cartilage; high levels of gicerin expression were observed in these cells. In the later embryonic and posthatching stages, no gicerin expression was detected in tracheal epithelium or cartilage. In addition, expression of gicerin increased transiently in the tracheal epithelium during the regeneration after tracheitis induced by the infectious bronchitis virus. Furthermore, a polyclonal antibody against gicerin inhibited the epithelial regeneration in tracheal organ cultures. These findings suggest that glcerin plays an important role in both tracheal development and regeneration.

Adult, professionally active patients with acute purulent tracheobronchitis were treated with azithromycin (3 or 5 days; n = 62) or clarithromycin (7 to 10 days; n = 69) in an open, randomized study. Bronchitis-related costs and treatment efficacy were assessed at day 5-6 and day 14-21. Both antibiotics were of equal clinical efficacy, although the median time to improvement of symptoms was significantly shorter for azithromycin patients than for clarithromycin patients. Some 77% of azithromycin patients and 78% of clarithromycin patients were unable to work for at least 1 day. The total time when patients were unable to work was shorter for azithromycin patients than for clarithromycin patients, but this difference did not remain significant when weekends and holidays were taken into account. Further studies are needed to assess the impact of azithromycin on time to clinical improvement, on lost working days, and on the associated costs.

1. The effects of formoterol, a beta 2-adrenoceptor agonist, on plasma protein exudation and microvascular permeability induced by topical, i.e. applied onto the tracheal mucosal surface, bradykinin (10 nmol; 20 microM, 5 min, 0.1 ml min-1) were studied in a perfused segment of trachea prepared in situ in anaesthetized rats. 2. Bradykinin increased the amount of plasma (fluorimetric assay for protein) in the perfusate (response; 10.98 +/- 0.357 microliters, n = 69; total increase in plasma over basal during 45 min after start of bradykinin application) and 2 responses at a 90 min interval were reproducible. Carbon labelling was seen in tracheal sections from animals that received i.v. colloidal carbon, indicating that bradykinin caused tracheal microvessels to leak (increase in microvascular permeability). 3. Five minutes after topical formoterol, 5 or 30 nmol (10 or 60 microM perfused for 5 min), the bradykinin response was significantly reduced. The effects of formoterol were not dose-related, i.e. were maximal at 5 nmol. The bradykinin response was at control levels 30 min after 5 nmol formoterol. After 30 nmol formoterol, the response was still reduced 120 min later. The bradykinin response was significantly reduced 60 min after systemic formoterol (i.p., 0.029 to 870 nmol kg-1) and, for 290 nmol kg-1 i.p. formoterol, this reduction was shown to last at least 150 min. 4 The bradykinin response was not prevented by supramaximal doses of topical (30 nmol) or i.p.(870 nmol kg-1) formoterol and carbon-labelled microvessels were seen in tracheal sections from all animals that received formoterol, although these were less in number and less densely labelled than in the absence of formoterol. There was a correlation between the plasma exudation response (ul) and the number of carbon-labelled vessels (Spearman's correlation coefficient 0.415, P<0.001).5 In animals pretreated with propranolol (3 pmol kg-1, i.v.), 29 nmol kg-1 formoterol, i.p., did not reduce the bradykinin response. However, propranolol itself markedly potentiated the bradykinin response which confounded the interpretation of its effects on formoterol.6 The study has shown, in a preparation of rat trachea in situ, that supramaximal doses of the beta2-adrenoceptor agonist, formoterol (a) produced a sustained, but incomplete, inhibition of plasma exudation (induced by topical bradykinin), and (b) did not prevent bradykinin-induced leaky microvessels. The data support the view that, at least in rodent airways, beta2-adrenoceptor agonists attenuate, but do not abolish, the microvascular permeability effects of bradykinin, a putative asthma mediator.

In neurogenic inflammation, tachykinins trigger the adhesion of neutrophils and eosinophils to leaky venules. The goals of the present study were to determine whether this leukocyte adhesion is mediated by neurokinin type 1 (NK1) receptors and to determine whether the amount of leukocyte adhesion corresponds to the amount of plasma leakage. Anesthetized rats were injected intravenously with substance P, the NK1 receptor agonist [Sar9, Met(O2)11]-substance P, or the NK2 receptor agonist [beta-Ala8]neurokinin A-(4-10). Five minutes later, the adherent neutrophils and eosinophils in blood vessels of the tracheal mucosa were stained histochemically and plasma leakage was quantified, as assessed by the extravasation of Monastral blue. Substance P and the NK1 agonist caused similar amounts of leukocyte adhesion, but the NK2 agonist had no effect. Pretreatment with the NK1 receptor antagonist CP-96,345 (4 mg/kg iv), before challenge with substance P, capsaicin, or aerosol hypertonic saline, reduced the amount of neutrophil adhesion by 56%, 93%, and 57% and reduced the amount of eosinophil adhesion by 70%, 83%, and 65%, respectively. Plasma extravasation was decreased by 89%, 95%, and 94%. The number of adherent neutrophils in the trachea was strongly correlated with the number of adherent eosinophils (r2 = 0.61). The greatest amount of leukocyte adhesion occurred in larger diameter venules than did the maximal amount of Monastral blue leakage. We conclude that NK1 receptors mediate the adhesion of neutrophils and eosinophils as well as the plasma leakage triggered by substance P, capsaicin, or hypertonic saline. This leukocyte adhesion evidently does not occur at exactly the same sites as the plasma leakage.

The purpose of this study was to identify a cohort of children with laryngotracheitis (croup) who may be safely discharged from the emergency department (ED) after treatment with nebulized racemic epinephrine (RE), corticosteroids, and prolonged observation. Consecutive children (younger than 13 years of age) presenting to the ED with the diagnosis of laryngotracheitis were evaluated prospectively according to a croup scoring system. Sixty-one patients (4 to 108 months of age) with persistent inspiratory stridor at rest after 20 minutes of mist therapy who received nebulized RE (0.05) mL/kg of a 2.25% solution) and intramuscular dexamethasone (0.6 mg/kg) were enrolled in the study. Patients were observed in the ED while croup scores were assessed at 15, 60, 120, and 180 minutes. Croup scores were significantly improved (analysis of variance, P < .01) throughout the observation period in 31 patients (51%) who were discharged from the ED. Only one patient returned within 48 hours for further cool mist therapy. The maximum benefit from RE therapy was seen at 60 minutes. If a child had persistent resting stridor or a croup score greater than 2 at that time, hospitalization was inevitable. The 30 patients admitted to the hospital were younger (19.1 v 27.8 months) and had higher pretreatment croup scores (5.7 v 4.1). This was the first prospective study to identify a subset of children who have received RE to be safely discharged home after observation in the ED.

The effect of alpha-trinositol (D-myoinositol-1,2,6-triphosphate) on edema formation and capillary permeability in neurogenically induced inflammatory edema was investigated in rat trachea. Interstitial fluid pressure (Pif) was studied, since increased negativity of Pif contributes to edema formation in this situation. alpha-Trinositol was used because it inhibits edema formation, capillary leakage, and increased negativity of Pif in burn-injured skin. Pif was measured with sharpened glass capillaries (3 to 7 microns) connected to a servocontrolled counterpressure system after circulatory arrest (induced by intracardiac injection of saturated potassium chloride in pentobarbital anesthesia). This was done in order to avoid the edema formation associated with inflammatory reactions, which will raise interstitial fluid volume and Pif, causing the underestimation of an increased negativity of Pif. Neurogenic inflammation induced by electrical-field stimulation of the left vagal nerve (10 V, 20 Hz, 0.5 ms) lowered Pif from -1.4 +/- 0.6 mm Hg to -8.4 +/- 2.1 mm Hg (p < 0.01). Corresponding numbers after the intravenous administration of alpha-trinositol (40 mg/kg) before stimulation were -1.2 +/- 0.4 and -1.4 +/- 0.4 mm Hg, respectively (p > 0.05). Another series of animals with intact circulation was used to study the effect of vagal nerve stimulation and alpha-trinositol on edema formation (total tissue water and extravascular 51Cr-ethylenediamine tetraacetic acid-[EDTA] space) and albumin extravasation. These parameters increased significantly after vagal nerve stimulation, while intravenous alpha-trinositol (40 and 120 mg/kg), as given above, significantly attenuated this increase. Thus, alpha-trinositol prevented a lowering of Pif and the edema formation accompanying neurogenic inflammation in rat trachea.

The present experiments were performed to investigate whether neurogenic inflammation in rat trachea (with edema formation and protein extravasation when the circulation is intact) induced by electrical field stimulation of neuropeptide-containing C fibers in the vagal nerve is accompanied by increased negativity of interstitial fluid pressure (P(if)). Increased negativity of P(if) in the trachea occurs in dextran anaphylaxis and mast cell degranulation and facilitates edema formation under these circumstances. Experiments were performed after circulatory arrest had been induced in pentobarbital anesthesia to prevent edema formation, which will raise P(if) and potentially cause underestimation of an increased negativity of P(if). After induction of circulatory arrest, the vagal nerve was isolated and placed in a stimulating electrode. The trachea was then exposed and covered with mineral oil, and measurement of P(if) was started as soon as possible thereafter. P(if) was measured with sharpened glass capillaries (tip diameter, 3 to 7 microns) connected to a servocontrolled counterpressure system. P(if) in the control group (n = 12) did not change throughout the observation period. Electrical stimulation of the left vagal nerve caused P(if) to fall in all experiments, from -1.1 +/- 1.1 mm Hg in the control condition to an average of -10.6 +/- 3.4 mm Hg (n = 9, P < .01). In some experiments, a continuous recording of P(if) was obtained, showing that the reduction of P(if) started within 30 seconds after onset of stimulation to reach and later remain at a stable level within a few minutes. The experimental protocol was repeated after the C fibers had been nearly depleted of neuropeptides with capsaicin.(ABSTRACT TRUNCATED AT 250 WORDS)

Retractions of the lower ribcage (chest wall distortion [CWD]) during inspiration are frequently observed with moderate to severe respiratory disease in the infant. Laryngotracheobronchitis (LTB) results in a reversible partial airway obstruction with severe CWD. We wished to measure the motion of the chest wall during distortion to determine the changes in minute ventilation (VE) and to evaluate this clinical sign as a means of assessing disease severity. The respiratory inductance plethysmograph was used to determine the distortion of the lower chest wall, and distortion was correlated with VE, measured at the mouth, in six infants with severe LTB and ventilatory failure. As the conditions of these infants improved, the CWD decreased with decreasing transcutaneous carbon dioxide tension (tcPCO2), VE increased from 0.27 +/- 0.12 L.min-1 x kg-1 at a tcPCO2 of 64 mm Hg to 0.64 +/- 0.06 L.min-1 x kg-1 when the tcPCO2 had fallen to 28 mm Hg. Over the same change in tcPCO2, the tidal volume (VT) increased from 4.8 +/- 0.5 ml.kg-1 to 15.7 +/- 1.4 ml.kg-1. In the most severe disease state, the excursion of the chest wall (as an inductance) was -14 +/- 3 mV in severe obstruction, but increased to 75 mV +/- 4 mV with resolution of the illness. The timing and vector of movement of the abdomen and chest wall were expressed as a Lissajous figure, which is measured as a phase angle. The severity of the disease process, as determined by tcPCO2 was directly related to the phase relationship, and thus reflected both VE and VT. The severity of the CWD may be assessed rapidly by the use of Lissajous figures.

Gastroesophageal reflux has been shown to play an important role in chronic and acute inflammatory disorders of the airway. In particular, gastroesophageal reflux has been suggested to be the cause of pharyngolaryngeal problems, according to the literature, at any age. However, to our knowledge, the presence of acid in the pharynx in pathological cases has not yet been proved. A series of eight patients (aged 2 months to 7.5 years) with recurrent acute laryngotracheitis underwent a two-channel pH monitoring for 23 to 24 hours. One pH probe was placed in the lower esophagus, the other in the pharynx, at the level of the epiglottis. Acid gastroesophagopharyngeal reflux was demonstrated in every patient. A significant difference with a series of six control subjects was noted in terms of esophageal and pharyngeal pH monitoring. The most significant item is the total time the pH in the pharynx was below 6. Despite the limited number of patients, this study suggests the role of gastroesophageal reflux in recurrent laryngotracheitis in infants and children.

A retrospective analysis was completed of the charts of the 1,727 patients with the diagnosis of croup seen during two years (1985 and 1986) in the Emergency Department of The Hospital for Sick Children in Toronto. Cough (91.4%) was the most common presenting symptom. Other presenting signs and symptoms included stridor (57.5%), chest wall retraction (38%), coryza and wheezing (18.5%) and tracheal tug (15%). The majority of patients were treated on an ambulatory basis while 377 (21.7%) were admitted for further management. Inpatient treatment included racemic epinephrine (120 patients) and parenteral steroids (17). Twelve (12) patients required airway support (endotracheal intubation). No tracheotomy for tracheitis was performed during this two year period. No deaths occurred in this patient population.

A major portion of airway blood flow is distributed to the subepithelial tissue space and is strategically located to influence both epithelial and airway smooth muscle functions. To assess the magnitude and responsiveness of blood flow through the subepithelial microvasculature, we measured tracheal mucosal blood flow with a soluble gas method in intact sheep. We found responses of tracheal mucosal blood flow to pharmacological stimuli alpha- and beta- (adrenoceptor agonists) and inflammatory stimuli (antigen and histamine), and demonstrated that alterations in mucosal blood flow influence the magnitude and duration of allergic airway smooth muscle contraction in the trachea. Mucosal blood flow, which under certain circumstances is regulated independently of total airway blood flow, could play a critical role in the manifestations of and recovery from airway disease.

DNA from calf thymus (1 to 10 micrograms/ml) was shown to stimulate the release of myeloperoxidase (MPO) and low amounts of H2O2 (about 1.5 nmoles/10(6) cells) from human polymorphonuclear leukocytes (PMNL). PMNL during 60 min incubation with DNA (10 micrograms/ml) and with DNA and cytochalasin B (4.8 micrograms/ml) released 14.4 +/- 3.4 and 25.5 +/- 4.8% (n = 7) of the total MPO cell activity, respectively. Higher DNA concentrations (0.25 to 1mg/ml) were chemotactic for PMNL as assayed under agarose method. At DNA concentration 1mg/ml the chemotactic index reached 1.5 +/- 0.2 and was approximate to value 1.7 +/- 0.2 (n = 7) obtained with zymosan-activated serum. However, the introduction of DNA to the mouse pleural cavity caused insignificant increase in the number of PMNL and lymphocytes recovered from the cavity at 3 h after injection, comparing it to material obtained from buffer-treated animals. The yield of DNA preparation from purulent sputum (about 10 micrograms/ml) indicates that DNA concentrations which activate PMNL in vitro occur in the inflammatory tracheobronchial secretion. The DNA from sputum electrophoresed on the 0.6% agarose gel reveal pattern which could be the result of nucleosomal DNA degradation. These results suggest that DNA released from nuclear debris in the place of inflammation, especially in the lower respiratory tract could secondarily modulate its course by PMNL activation. This novel role of DNA may be important for pulmonary pathology since lungs are susceptible to proteolytic and oxidant mediated injury.

The problem of endotracheal erosion associated with neonatal high-frequency jet ventilation (HFJV) is investigated through measurement of air velocity profiles in a scaled up model of the system. Fluid mechanical scaling principles are applied in order to construct a model within which velocity profiles are measured by hot-wire anemometry. The effects of two different jet geometries are investigated. Velocity gradients measured near the tracheal wall are used to measure the shear stresses caused by the jet flow on the wall. The Chilton-Colburn analogy between the transport of momentum and mass is applied to investigate tracheal drying caused by the high shear flow. Shear forces are seen to be more than two times higher for jets located near the endotracheal tube wall than for those located axisymmetrically in the center of the tube. Since water vapor fluxes are dependent on these shears, they are also higher for the asymmetric case. Fluxes are shown to be greatly dependent on the temperature and relative humidity of the inspired gas. Water from the tracheal surface may be depleted within one second if inspired gases are inadequately heated and humidified. It is recommended that the design of neonatal HFJV devices include delivery of heated (near body temperature), humidified (as close to 100% humidity as possible) gases through an axisymmetric jet to best avoid the problem of endotracheal erosion.

The reactivity of cat tracheal smooth muscle to histamine in vitro was studied at various degrees of inflammation of the airways induced experimentally by the intratracheal administration of turpentine oil or Staphylococcus aureus, both in aerosol form. Tracheal smooth muscle preparations from the control animals did not respond to histamine in doses of 10(-9)-10(-3) mol X 1(-1). In tracheal preparations from three groups of cats with turpentine oil inflammation induced 24 h, 48 h and 15 days previously, histamine caused contractions in 20, 70 and 24% of the cats, respectively, according to the degree of inflammation. All tracheal preparations from cats with staphylococcal inflammation responded to histamine by contraction. Atropine, acetylosalicylic acid and phentolamine did not abolish histamine contractions in tracheal preparations, but clemastine did.

Quantitative clearance of aerosolized Escherichia coli from the trachea, lung, and air sacs was measured in turkeys infected with Bordetella avium. Clearance of E. coli in turkeys with B. avium-induced tracheitis was minimally affected early in infection. Sixteen to 23 days after infection with B. avium, sporadic, mild depressions in clearance of E. coli were observed in the tracheas, which had large areas of deciliated tracheal epithelium or replacement of normal epithelium by immature hyperplastic epithelium or metaplastic squamous epithelium. Clearance of E. coli from the lung and air sacs was minimally affected in turkeys infected with B. avium.

The authors describe changes in the cough reflex in unanaesthetized cats with experimental local tracheitis. Inflammation was produced by a silk suture fixed in the trachea and cough was elicited by mechanical stimulation of different parts of the respiratory tract mucosa. The resultant cough values (the number of efforts, the intensity of the maximum effort and the intensity of the attack) were compared with the corresponding values in healthy cats. In animals with a tracheal suture, inflammation was confined to the trachea. The intensity of cough elicited by stimulation of this region increased significantly compared with normal (on the 15th to 17th day of inflammation), whereas cough elicited from the laryngopharyngeal and tracheobronchial region did not. On about the 20th day of inflammation the authors found a decrease in the intensity of the maximum effort of cough elicited from the inflamed part of the trachea and a decrease in the intensity of the maximum effort and the intensity of the coughing attack elicited from the laryngopharyngeal and tracheobronchial region. They assume that the decrease could have been due to the development of protective inhibition in central structures participating in integration of the cough reflex.

The present study was performed to determine whether neurogenic inflammation in the rat trachea can be exaggerated by inhibiting neutral endopeptidase, an enzyme that degrades tachykinins that are believed to mediate neurogenic inflammation. Neurogenic inflammation was produced by antidromic electrical stimulation of one vagus nerve (2.5 Hz, 1 ms, 5 V for 5 min) in the presence of atropine or by an intravenous injection of capsaicin (100 micrograms/kg). Neutrophils that adhered to the endothelium of venules were visualized and counted in tracheal whole mounts that were stained by a histochemical reaction for myeloperoxidase. Neural inflammation increased the number of adherent neutrophils. Pretreatment with the neutral endopeptidase inhibitor phosphoramidon (1.0 or 2.5 mg/kg iv) increased neutrophil adhesion induced by neural inflammation. As assessed by the amount of extravasation of Monastral blue pigment, neural inflammation also increased vascular permeability, and this change was potentiated by phosphoramidon. These results are consistent with the concept that neuropeptides released from sensory nerves in the tracheal mucosa cause neutrophils to adhere to venules and increase vascular permeability and that these effects are modulated by neutral endopeptidase.