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Nubp1 (also known as Nbp35) and Nubp2 (also known as Cfd1) proteins are known to be responsible for regulating centrosome duplication in mouse and ribosome biogenesis in yeast. Nubp proteins contribute to diverse physiological functions. It is thought that Nubp1 and Nubp2 proteins interact with each other and regulate their functions. However, little is known about the intracellular localization of Nubp proteins. In this study, we compared the intracellular localization of human Nubp1 and Nubp2 by fusing these proteins with green fluorescent protein (GFP) in HeLa cells. The nuclear transfer of Nubp1-GFP, where GFP was fused to the C-terminus, was not observed. However, GFP-Nubp1, where GFP was fused to the N-terminus, did accumulate in the nucleus. In addition, GFP-modification at the N-terminal of Nubp2 induced nuclear transformation. Our data suggest that the C-terminal region of Nubp1 is important for nuclear transfer and the N-terminal of Nubp2 contributes to the morphology of the nucleus.

The functional residual capacity (FRC) and airway resistance (R(aw)) of the rat were measured, using a newly designed body plethysmograph (BPG), the inner environment of which was maintained at body temperature and was water-vapor saturated. The subjects were anesthetized and tracheally intubated male Wistar rats (n = 15). After measuring the FRC and R(aw), we analyzed the effects of inhaled methacholine (Mch, 0-8 mg/ml) on R(aw).The determined FRC was 5.37 +/- 0.22 ml (mean +/- SE). An almost linear relationship between box pressure and respiratory flow was obtained when the difference between box-gas temperature and the rectal temperature of the rat was less than 1.0 degrees C. The R(aw) at FRC was 0.230 +/- 0.017 cm H(2)O/ml/s. It increased proportionally with increases in the Mch concentration. When the dynamic changes in R(aw) were analyzed, the R(aw) was found to progressively increase during expiration; this increase continued throughout inspiration. Thus in the rat, R(aw) is not simply a function of changes in lung volume. In conclusion, the humidity- and temperature-adjusted BPG provided an absolute and possibly dynamic value of R(aw).

A synchronous evaluation was performed, using a quick in vivo [2-(14)C]thymidine labeling method, of the toxico- and pharmaco-dynamics of a given dose of yttrium-90 (90Y) at a given time after injection to nude BALB/c mice loaded with 10(7) HuO9 cells. Quantitative data were 14C-microautoradiographs of the liver lobule, intestinal crypts, epiphysial growth plate, secondary ossification center containing pluripotent stem cells, perifollicular zone containing unipotent stem cells in the spleen, and plasmacytoma cells in the osteogenic sarcoma in each mouse following a 10-min labeling with 14C at 0.5, 6, and 24 h after i.v. injection of 90Y. Results show that the cell proliferation rate of the stem cells in respective tissues was markedly suppressed, dependent on time after dosing and the dose of 90Y; 3.7, 37, 370, 3700, and 37,000 kBq per mouse (25 g). In addition to the above, the sensitivity of the proliferation rate was dependent on amitosis or mitosis and the AUC value of 90Y-concentration at specific locations of the cells in the mouse body. The most sensitive cells were the plasmacytoma cells, followed by the pluripotent and unipotent stem cells, the intestinal crypts, epiphysial growth plate, and liver cells.

To interpret the MRI signal intensities, the T1 and T2 values were determined in vitro for rat lungs with radiation pneumonitis, fibrosis or pneumonia, and also for muscle and fat tissues. The transverse magnetization decays mentioned above exhibited two components, a T2 fast (T2f) and a T2 slow (T2s) component. Lungs from rats with pneumonia had significantly longer T2f and T2s values than lungs from rats with radiation pneumonitis and fibrosis. The T2f and T2s values for a "pneumonia lung" were not significantly different from those of muscle. The measured values of T2f and T2s suggested that radiation pneumonitis and fibrosis likely exhibit lower signal intensities than do muscle and that a "pneumonia lung" likely exhibits a similar signal intensity to that of muscle on T2-weighted MR images.

We recently developed a method of proton magnetic resonance spectroscopy (1H-MRS) to measure the 1H-MR spectra of peripheral blood lymphocytes (PBL) using only 10(7) cells. We investigated the clinical feasibility of this method for evaluating disease activities in sarcoidosis and interstitial pneumonitis. PBL was separated from 10 ml of venous blood by differential centrifugation with Ficoll-Conray. Using a 90 MHz MR spectrometer (EX90, JEOL), the spectrum was obtained with 4000 times accumulation of 1H signals by single 70 degree pulses at 37 degrees C under spinning. Water signal was suppressed with the homo-gated decoupling sequence. The spectra were analyzed with Gaussian curve fitting. The spectra of patients with active disease showed significant increases in peak heights for (CH2)n and CH3 peaks compared with the control. The peak heights decreased after improvement of disease states. The changes in 1H-MR spectra suggested activation of PBL in patients with sarcoidosis and interstitial pneumonitis, since similar changes have been shown for cells activated with mitogens. Our preliminary results indicate that 1H-MRS may be useful to evaluate activation of PBL in sarcoidosis and interstitial pneumonitis.

It remains unknown how increased upper airway resistance (UAR) during sleep could be a function of gravity. We therefore conducted quantitative evaluation of the gravitational influence on diaphragmatic EMG activity (EMGdi) in an astronaut to estimate the effect of UAR in space. EMGdi was recorded by paired surface electrodes on the ground (control, C) and abroad a short-term space mission (space, S) for 30 consecutive h. Mean EMGdi recorded during quiet breathing in wakefulness was assigned the value of 100. EMGdi in C was significantly enhanced in all sleep stages compared with that while awake in the supine position (mean +/- SD, 230 +/- 23.2% in non-rapid eye movement (non-REM) Stage II, 233 +/- 13.8 in slow-wave sleep, and 233 +/- 40.0 in REM sleep versus 100 +/- 17.3 in wakefulness, p < 0.001). In contrast, there was no statistical difference in EMGdi in S between awake and any non-REM sleep stage (mean +/- SD, 100 +/- 20.5% in wakefulness versus 103 +/- 16.9 in non-REM Stage II and 100 +/- 14.8 in slow-wave sleep; NS). However, EMGdi in REM sleep in S was statistically greater (132 +/- 28.3%) than that during wakefulness or any other sleep stage in space (p < 0.001). Therefore, gravity may play a much more significant role in the normal healthy human in the increased upper airway resistance during sleep than the relative atonia of the upper airway muscles.

A 74-year old male was referred to the Tokai University Hospital for evaluation of abnormal opacities on a chest roentgenogram. Laboratory tests demonstrated leukocytosis, elevated ESR and CRP, elevated LDH, and hypoxemia. The chest roentgenogram demonstrated several ill-defined nodular infiltrates on the bilateral upper lung fields. In addition, a CT scan revealed bilateral pleural effusion which was found bloody on diagnostic thoracocentesis. Administration of antibiotics failed to improve lung infiltration or laboratory data. The patient died of respiratory failure on the 23rd hospital day. At autopsy, multiple ill-defined nodules, which were associated with alveolar hemorrhage, were scattered in the lungs bilaterally. Both hematoxylin-eosin and silver staining showed atypical cells of a vasoformative nature. Factor VIII related-antigen in the tumor cells was confirmed by the peroxidase-antiperoxidase method. These findings were consistent with angiosarcoma. The tumor foci were demonstrated in the lungs, pleura, kidneys, bone marrow, adrenal glands, and the gastrointestinal tract. The primary site of angiosarcoma, however, was not identified. Angiosarcoma, either primary or metastatic to the lungs, should be included in the differential diagnosis of multiple ill-defined nodular opacities associated with hemothorax.

We report a 71-year-old female patient with primary alveolar hypoventilation syndrome who received diaphragm pacing (DP) and developed obstructive sleep apnea syndrome (OSAS). Application of nCPAP markedly improved her nocturnal hypoxemia. The monitored polygrams before and after the application strongly suggested that the main mechanism of OSAS was an imbalance of activity between upper airway dilator muscles and pump muscles. Moreover, paradoxical movement of the rib cage is not necessarily due to upper airway obstruction. Monitoring of tidal volume and arterial oxygen saturation is essential for the diagnosis of DP-induced OSAS.

To evaluate the energy metabolism of peripheral skeletal muscle during exercise in patients with chronic respiratory impairment, the 31P-nuclear magnetic resonance (NMR) spectra of forearm muscle were investigated in nine patients and nine age-matched control subjects. We calculated the phosphocreatine (PCr) to PCr + inorganic phosphate (PI) ratio, the time constant of PCr recovery and the intracellular pH. The exercise consisted of repetitive hand grips against a 2-kg load every 3 s for 6 min (0.33 W). The patients showed a marked decrease in the PCr/(PCr + PI) ratio and pH in the muscle during exercise in contrast to the control subjects whose PCr/(PCr + PI) showed a minor decrease without any change in pH. The relationship between PCr utilization and pH demonstrated that anaerobic glycolysis switched on earlier in patients with chronic respiratory impairment. A split PI peak was observed in five of nine patients during exercise. The PCr/(PCr + PI) ratio during the last minute of exercise correlated significantly with the vital capacity (% predicted), with the FEV1/FVC, with the body weight, with the maximum strength of hand grip, and with the muscle mass. The results indicate impaired oxidative phosphorylation and the early activation of anaerobic glycolysis in the muscles of patients with chronic respiratory impairment. Several factors related to chronic respiratory impairment, such as disuse, malnutrition and dysoxia, would contribute to the metabolic changes observed in the muscles examined.

The role of reperfusion injury in the progression to necrosis in pulmonary embolism was evaluated. To simulate this condition, we used a technique that enables occlusion and reopening of the pulmonary arterial branch supplying the right upper lobe in conscious rats. The rats were divided into five groups: the occlusion group (n = 12), in which the pulmonary artery (PA) branch was occluded without reperfusion; the reperfusion group (n = 12), in which the PA branch was reopened after a 2-h period of occlusion; and the reperfusion-SOD (n = 9), reperfusion-IM (n = 8), or reperfusion-IA-SOD (n = 6) groups, in which superoxide dismutase (SOD), indomethacin (IM), or inactivated SOD (IA-SOD), respectively, was administered during reperfusion. The lungs were removed 24 h after the PA occlusion, and histologic examination was performed. In the occlusion group, the alveolar structure of the right upper lobe was well preserved, and there was no erythrocyte or leukocyte accumulation. The only significant changes compared with the control lobe was the appearance of wavy internal elastic lamina of the PA and slight neutrophil adherence to the endothelial cells. In contrast, the right upper lobe of the reperfusion group disclosed numerous foci of hemorrhagic necrosis, with disrupted alveoli and leukocyte accumulation in all cases. With SOD treatment, the changes compatible with hemorrhagic necrosis were attenuated to the level of the control lobes. However, neither IM nor IA-SOD decreased these changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Activity of the respiratory muscles during natural defecation was studied in two anesthetized and two decerebrate dogs. In anesthetized dogs, excitation of the abdominal muscles and an increase in gastric pressure were observed during defecation. However, pleural pressure was little influenced by such increase in abdominal pressure, maintaining the same rhythmic changes as observed during spontaneous respiration. The rhythmic changes in pleural pressure were associated with rhythmic activity of the diaphragm. When gastric pressure increased during defecation, the diaphragmatic activity also increased during both the inspiratory and expiratory phases. In a decerebrate dog, airflow and airway pressure changed similarly to during defecation. The diaphragm was continuously active, with superimposed rhythmic augmentation. In a paralyzed and artificially ventilated dog with open-chest, the phrenic nerve similarly developed discharges. We conclude that the non-respiratory activity and rhythmic augmentation of phrenic nerve discharge during defecation is pre-programmed in the command for defecation. The activity of phrenic motoneurons may be further modulated by changes in thoracic and abdominal pressure. These mechanisms may act together to coordinate respiration and defecation.

Abscess formation is uncommon in eosinophilic lung disease. In this paper we present a case of chronic eosinophilic pneumonia in which bronchofiberoscopy revealed scattered small abscesses in the large airways. Pathological examination revealed the presence of inflammatory cells with eosinophilic infiltration in both the bronchial mucosa and lung parenchyma.

A 38-year-old man was admitted with persistent productive cough and right anterior chest pain. Chest X-ray showed two large masses connected with each other, one in the right lung field and the other in the anterior mediastinum. A tentative diagnosis of either lung abscess or bronchogenic carcinoma was initially made, because of elevated serum tumor markers (SLX and SCC) and persisting refractory inflammatory sings. However, open chest drainage revealed a few fine hairs and atheromatous materials within the masses, and the diagnosis of teratoma was made. We removed these masses, and investigated the reason for the elevation of tumor markers. Staining with SLX monoclonal antibody demonstrated that the pancreatic tissue in the masses contained SLX. Although this is the first reported case of teratoma producing tumor marker (SLX), it is highly possible that tumor markers may be elevated in the majority of patients with teratoma because of the genesis of this tumor.

To investigate the neural mechanism of the expiratory activity of the inspiratory muscles during a cough, EMG of the respiratory muscles were recorded in anesthetized and tracheostomized dogs. A laparoscope was used to minimize injury to the abdominal muscles for implantation of the electrodes into the costal diaphragm. During the expulsive phase of a cough, the diaphragm was active in 7 of 12 dogs and the external intercostal muscle was active in 3 of 6 dogs. During a cough, the expiratory activity of the diaphragm, after the termination of its inspiratory activity, started at 52.9 +/- 24.6 ms, and that of external intercostal muscle started at 51.1 +/- 20.5 ms. The expiratory activity of the internal intercostal muscle and of the transversus abdominis started at 34.3 +/- 13.0 and 27.8 +/- 15.2 ms, respectively. The onset of expiratory activity of the inspiratory muscles is significantly later than that of expiratory muscles. Continuous activity in the expiratory muscles evoked by airway occlusion, i.e., Hering-Breuer reflex, was suppressed during the inspiratory phase of a cough, but not suppressed during the expulsive phase even when the expiratory activity of the diaphragm was observed. We concluded that the expiratory activity of inspiratory muscles is controlled independently of both expiratory activity of the expiratory muscles and inspiratory activity of the inspiratory muscles.

We report a case of a 61-year-old male without any predisposing factors. His X-ray film showed multiple nodular lesions in bilateral lung fields. Open lung biopsy revealed Zygomycetes in the granuloma. The patient was treated with amphotericin B and miconazole, and remains alive more than 32 months later.

Cough responses evoked by mechanical stimulation of the tracheobronchial mucosa in anesthetized and tracheostomized dogs were studied. The most common response was a group of coughs. Phase relationships between coughing and spontaneous respiration during the cough initiation and resolution periods were categorized as either synchronized or unsynchronized. We defined the synchronization as the coincidence of an expiratory thrust and the early-expiratory phase of respiration. During the cough initiation period, the incidence of synchronization increased as central respiratory activity was enhanced by hypercapnia or as the cough center's activity was suppressed by deep anesthesia. Synchronization decreased as central expiratory activity was enhanced by expiratory threshold loading. During the cough resolution period, synchronization occurred in conjunction with a gradual decrease in the cough center's activity. Coughing could be evoked when the dog was made apneic either by hyperventilation or by the Hering-Breuer reflex. In either case, apnea persisted after coughing subsided. These findings suggest that mechanical stimulation directly activates the cough center rather than the respiratory center; and that synchronization is determined by the relative strengths of the respiratory and cough center's activities.

Inhalation anesthesia first with halothane followed by enflurane relieved a patient with status asthmaticus who was refractory to conventional therapy including mechanical ventilation. After 13 days of anesthesia while on mechanical ventilation and employing nondepolarizing muscle relaxants, significant neuromuscular impairment, manifested by tetraplegia and sensory disturbance, developed. Anesthesia was discontinued on day 14, and the patient was weaned from mechanical ventilation on day 16. Over the next two months, the neuromuscular impairment markedly improved. Halothane was associated with cardiac arrhythmias and hepatitis necessitating replacement by enflurane. Enflurane appeared to be as effective a treatment for refractory asthma as halothane. The most probable cause of the neuromuscular impairment in our patient was the long-term use of inhalation anesthetics or nondepolarizing muscle relaxants.

NMR relaxation times (T1 and T2) and the water content (WC) of in vitro rat lungs were measured during the course of endotoxin lung injury in rats. Measurements of normal lungs, untreated endotoxin-injured lungs, and endotoxin-injured lungs treated with methylprednisolone (MPSL) were compared. The untreated endotoxin lungs showed prolongation of the fast and slow T2 components (T2f and T2s), but no significant changes in T1 or water content. Also, there was no correlation between 1/WC and relaxation rates or between T1 and T2. MPSL treatment prevented T2f and T2s prolongation; however, the duration of MPSL effectiveness was limited. Animals which were treated with MPSL more than 7 h prior to measurements showed T2 prolongation. This study indicates that NMR relaxation times, particularly T2, can be useful in evaluating lung injuries and their treatments.

To investigate the NMR relaxation times for irradiated rat lung tissue, we measured T1 and T2 at 11 different times during the injury's 1-year time course. A biexponential analysis of T2 was used to determine T2 fast (T2f) and T2 slow (T2s). In addition, we measured water content and correlated changes in the relaxation times with pathological changes. The correlation indicates the following: (1) Shortly after irradiation, the biexponential T2 decay for 1/3 of the samples became monoexponential and there were no noticeable pathological changes observed using light microscopy. (2) During radiation pneumonitis, T2f and T2s were prolonged. This accompanied acute edematous changes and inflammatory cell infiltration. (3) Finally, during radiation fibrosis T1 shortened and collagen increased. We observed no significant correlation between relaxation time changes and water content changes throughout the 1-year time course.

A 18-year-old female complained of a dyspneic sensation and involuntary movements in the epigastrium. On physical examination, fine rhythmic movements in the epigastrium were observed on each inspiration with a rate of 5-10 per breath. Arterial blood gas analysis was normal. Recording of the respiratory parameters and the EMG of respiratory muscles were performed. Analysis of the respiratory flow revealed that her spontaneous inspirations consisted of short inspirations (i.e., flutter wave) (150-170 beats per minute). EMG of respiratory muscles demonstrated that these flutter waves were driven by intercostal muscles and diaphragm. The flutter waves were not suppressed by breath holding at the maximal inspiration. With intravenous injection of 200 mg of diphenylhydantoin, flutter waves disappeared within 10 minutes. There were no abnormal findings on chest roentgenogram, electrocardiogram, head CT scan and MRI of the cervical spine. During one year's follow up no attack developed again. We have encountered 3 cases of the syndrome since 1981. In two of them, the spontaneous respiration was superimposed on a high-frequency wave throughout the whole respiratory cycle while in one case the high-frequency wave developed only in the inspiratory phase of spontaneous respiration. In the present case the respiratory flow pattern was similar to the last mentioned and the EMG-analysis of respiratory muscles confirmed that the flutter waves were driven by intercostal muscles and diaphragm. Furthermore, synchronization of activities of the two respiratory muscles suggests that the syndrome is of central origin.

Control mechanism of the respiratory muscle during forced expiration was analyzed. Respiratory flow. EMG of the intercostal muscle (IC), external oblique (EO) and internal oblique (IO) abdominal muscle were analyzed in eleven healthy volunteers. The pattern of EMG activity during forced expiration could be classified according to its shape i.e., taper- or hill-shaped. The taper shape was found in 7 of 9 subjects for IC and in 8 of 11 subjects for EO. The hill shape was found in 4 of 6 subjects for 10. Twelve consecutive trials without intervals did not alter the pattern of flow-volume curve, activity of respiratory muscle and frequency component (i.e., H/L ratio). When the expiratory circuit was obstructed for a short interval during forced expiration, the rise in pleural pressure was slight but that in oral pressure was large, and the activity of respiratory muscle decreased for a short period. The latencies from the onset of expiratory circuit obstruction to the reduction in EMG activity were 61.5-100 msec. In IC, 61.5-106.5 msec in EO. and 58.0-92.3 msec in 10. These values did not differ significantly any given subject. Airway anesthesia with xylocaine did not alter latency. In conclusion, the pattern of respiratory muscle activity for forced expiration is predetermined and is specific for each muscle. Negative feedback from receptors in airway or in respiratory muscle was strongly suggested. Repetitive trials up to twenty times did not cause respiratory muscle fatigue.

A 23-year-old woman developed acute respiratory failure in the course of multiple sclerosis. The lack of bulbar dysfunction, the presence of quadriplegia, and the bilateral diaphragmatic weakness indicated the presence of spinal cord lesions involving pyramidal tracts bilaterally. Magnetic resonance imaging revealed a cervical demyelinating lesion between C1 and C3.

Continuous positive airway pressure (CPAP) breathing of 10 cmH2O was applied to 10 healthy conscious subjects both in supine and 70 degree head-up postures. CPAP increased the end-expiratory lung volume from 2.44 +/- 0.66 (S.D.) to 3.07 +/- 0.68 liters in supine subjects, and from 3.01 +/- 0.57 to 3.64 +/- 0.57 liters in head-up subjects. During CPAP, rib cage motion became predominant when compared to abdominal motion in upright posture. Among the respiratory parameters, inspiratory duration was significantly shortened during CPAP in either posture, but was changed less significantly by individual posture change alone. Mean inspiratory flow decreased during CPAP only in upright posture. Abdominal muscles were recruited for expiration during CPAP in either posture, and the EMG recorded from the lower intercostal space developed inspiratory activity during CPAP in head-up posture. All of 10 subjects felt most dyspneic during CPAP with the head-up. We conclude that the mechanism of increase in lung volume during CPAP is mediated by different pathway from that of posture change, and that CPAP in upright posture can alter the respiratory pattern of the subject.

Paraquat poisoning has been associated with very high mortality. The toxic mechanism is considered to be related to the production of superoxide ions. Review of the literatures reveals that with vigorous treatment recovery from poisoning is not impossible. Clinical experience in four cases of paraquat poisoning and the principles of management of this intoxication are presented.

We investigated changes in the pulmonary carbon monoxide diffusing capacity (DLco) during the cold pressor test (CPT) on 25 normal subjects. In 10 of them we also observed changes in circulatory parameters by a computerized dual cadmium telluride detector system, using an equilibrium radionuclide blood-pool label. DLco and DLco per unit of alveolar volume (DLco/VA) averaged in the control period were 29.4 +/- 4.1 ml/min/mm Hg, 6.1 +/- 0.8 ml/min/mm Hg/l (mean +/- SD). During the 2nd minute of CPT, DLco increased by 3.6 +/- 1.5% and DLco/VA by 5.1 +/- 1.5% (mean +/- SE). The systemic blood pressure increased by 17% (mean increase) whereas the heart rate and the stroke volume remained unchanged. The increases were small but significant (p less than 0.05, p less than 0.01, respectively). We conclude that the increase in DLco is due to cold-induced systemic vasoconstriction followed by a passive shift of blood into the pulmonary vasculature.

Proton magnetic relaxation times, T1 and T2, were determined for rat lungs exposed to 80% oxygen for a duration of 2 weeks. The transverse magnetization decay curve of the lung tissue was multiexponential. A linear combination of two decay curves with different T2 values fits the multiexponential decay suggesting that there are at least two different components of tissue water in the lung. Remarkable prolongation of T1 and T2 was demonstrated as lung injuries progressed in the acute stage of pulmonary edema. Both 1/T1 and 1/T2 were significantly correlated with 1/water content of the lung tissue. In the repair stage, T1 and T2 were significantly shortened. Shortening coincided with the spontaneous resolution of pulmonary edema. Relaxation rates showed no significant correlation with 1/water content in this stage. These results indicate that the physical state of water in the tissue is affected not only by the water content but also by the derangement of macromolecules in pulmonary edema. T2 was more sensitive than T1 for detecting pulmonary damage.

Neural mechanisms regulating activities of diaphragm and abdominal muscles were investigated on anesthetized, tracheostomized and spontaneously breathing dogs. EMGs of costal diaphragm and external oblique (EO)abdominal muscle were recorded by fine-wire electrodes. The electrodes for diaphragm-EMG were implanted without opening abdominal cavity using laparoscopy. During quiet breathing the mean firing frequency of diaphragm-EMG was 7.6 +/- 0.7 (S.D.) Hz. The discharge spikes of diaphragm-EMG observed in early-inspiration or in post-inspiratory phase, were low in amplitudes, consistent with previous reports that phrenic motoneurons were comprised of two populations. During quiet breathing spikes were not observed in EO-EMG in a half of the animals, and were tonically-firing in the remaining dogs. Hypercapnia increased firing frequency of diaphragm-EMG, but did not recruit spikes of high amplitude. On the other hand, hypercapnia recruited EO-spikes of higher amplitude, and increased firing frequency. When spikes fired tonically in EO-EMG, hypercapnia suppressed these spikes during inspiration. Airway occlusion gradually recruited EO units of higher amplitude. Mechanical stimulation of upper airway suppressed tonic-EO activity during inspiration. In conclusion, we demonstrated that 1) abdominal wall is not related with control mechanism of diaphragm; 2) the control mechanism of dog's EO differs from cat's internal intercostal muscles; and 3) the tonic component of EO is affected by respiratory commands from higher neuronal architecture.