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The rise in pellet consumption has resulted in a wider variety of materials for pellet manufacture. Thus, pellet industry has started looking for alternative products in relation to wood biomass, such as wastes from agricultural activities, and related industries, along with the combination thereof, obtaining a broad range of these products. The results of the experiment showed significant differences between the analyzed biomass fuels burned under different operating conditions in a laboratory reactor with a model circulating bed. These differences are mainly associated with problematic phenomena during combustion, including sintering of ashes.

Agricultural residual biomass presents a high potential for energy use around the world, often not utilized to a large extent due to its significant differences with respect to other biomass types, such as the one of wood origin. These differences are mainly related to the characteristics of its ashes (quantity and composition) which increase certain problematic phenomena during combustion, among them ash sintering. The main purpose of this article is the experimental study of these issues for various agro pellets and wood pellets, analyzed in various operating conditions in a laboratory reactor with a circulating bed.

In the present research long-term pulmonary toxicity of lead was investigated in rats treated by intraperitoneal administration of lead acetate for three consecutive days (25 mg/kg per day). Five weeks after treatment average lead content in the whole blood was 0.41 μg/dL ± 0.05, in the lung homogenates it measured 3.35 μg/g ± 0.54, as compared to the control values of 0.13 ± 0.07 μg/dL and 1.03 μg/g ± 0.59, respectively. X-ray microanalysis of lung specimens displayed lead localized mainly within type II pneumocytes and macrophages. At the ultrastructural level the effects of lead toxicity were found in lung capillaries, interstitium, epithelial cells, and alveolar lining. Alveolar septa showed intense fibrosis, consisting of collagen, elastin, and fibroblasts. Thinned alveolar septa had emphysematous tissue with some revealing signs of angiogenesis. Type II pneumocytes contained lamellar bodies with features of laminar destruction. Fragments of the surfactant layer were often detached from the alveolar epithelium. These findings indicate that 5 weeks after exposure, lead provokes reconstruction of the alveolar septa including fibrosis and emphysematous changes in the lung tissue.

The purpose of our study was to determine the cardio-respiratory pattern exerted by the systemic injection of neurotensin, contribution of neurotensin NTS(1) receptors and the neural pathways mediating the responses. The effects of an intravenous injection (i.v.) of neurotensin were investigated in anaesthetized, spontaneously breathing rats in following experimental schemes: (i) control animals before and after midcervical vagotomy; (ii) in three separate subgroups of rats: neurally intact, vagotomized at supranodosal level and initially midcervically vagotomized exposed to section of the carotid sinus nerves (CSNs); (iii) in the intact rats 2 minutes after blockade of neurotensin NTS(1) receptors with SR 142948. Intravenous injection of 10 μg/kg of neurotensin in the intact rats evoked prompt increase in the respiratory rate followed by a prolonged slowing down coupled with augmented tidal volume. Midcervical vagotomy precluded the effects of neurotensin on the frequency of breathing, while CSNs section reduced the increase in tidal volume. In all the neural states neurotensin caused significant fall in mean arterial blood pressure preceded by prompt hypertensive response. The cardio-respiratory effects of neurotensin were blocked by pre-treatment with NTS(1) receptor antagonist. The results of this study showed that neurotensin acting through NTS(1) receptors augments the tidal component of the breathing pattern in a large portion via carotid body afferentation whereas the respiratory timing response to neurotensin depends entirely on the intact midcervical vagi. Blood pressure effects evoked by an intravenous neurotensin occur outside vagal and CSNs pathways and might result from activation of the peripheral vascular NTS(1) receptors.

The respiratory effects of stimulation of NPYY 2 receptors were studied in spontaneously breathing rats that were either (i) neurally intact and subsequently bilaterally vagotomized in the neck, or (ii) neurally intact and subjected to supranodosal vagotomy or (iii) neurally intact treated with pharmacological blockade of NPY 1–2 receptors. Before neural interventions an intravenous (iv) bolus of the NPYY 2 receptor agonist NPY 13–36 (10 μg/kg) increased breathing rate, tidal volume and mean arterial blood pressure (MAP). Section of the midcervical vagi abrogated NPY 13–36-evoked increase in respiratory rate but had no effect on augmented tidal volume, minute ventilation and blood pressure. Supranodosal vagotomy prevented the increase in tidal volume and slightly reduced the pressor response. Blockade of NPYY 2 receptor with intravenous doses of BIIE 0246 eliminated cardio-respiratory effects of NPY 13–36 injection. BMS 193885 – an antagonist of NPYY 1 receptor-was not effective in abrogating cardio-respiratory response. The present study showed that (i) NPY 13–36 induced stimulation of breathing results from activation of NPYY 2 receptors associated with pulmonary vagal afferentation; (ii) the increase in the frequency of breathing is mediated by midcervical vagi and augmentation of tidal volume relies on the intact supranodosal trunks (iii) the pressor response results from the excitation of NPYY 2 receptors outside of the vagal pathway.

Pulmonary toxicity of lead was studied in rats after an intraperitoneal administration of lead acetate at a dose of 25 mg/kg. Three consecutive days of treatment increased lead content in the whole blood to 2.1 µg/dl and in lung homogenate it attained 9.62 µg/g w.w. versus control values of 0.17 µg/dl and 0.78 µg/g w.w., respectively. At the ultrastructural level, the effects of lead toxicity were observed in lung capillaries, interstitium, epithelial cells and alveolar lining layer. Accumulation of aggregated platelets, leucocytic elements and monocytes was found within capillaries. Interstitium comprised a substantial number of collagen, elastin filaments and lipofibroblasts. Lamellar bodies of type II pneumocytes contained phospolipid lamellae, which stratified into an irregular arrangement. Pulmonary alveoli were filled with macrophages. The extracellular lining layer of lung alveoli was partially destroyed. This study provided evidence that acute lead intoxication affects the whole lung parenchyma and by impairing production of the surfactant might disturb the regular respiratory function.

The respiratory effects evoked by systemic injection of neuropeptide Y (NPY) were studied in anaesthetized, spontaneously breathing rats that were (i) neurally intact; (ii) subjected to bilateral midcervical vagotomy (MC vagi cut); (iii) midcervically vagotomized and treated by supranodosal denervation (NG vagi cut); (iv) neurally intact, before and after pharmacological blockade of the NPY Y 1 and NPY Y 2 receptors. An intravenous (iv) bolus of NPY (100 μg/kg) induced slowing down of the respiratory rate, decreased tidal volume and heart rate, and increased mean arterial blood pressure. After section of midcervical vagi, NPY still evoked the cardio-respiratory changes. Supranodose vagotomy abolished the fall in respiratory rate and reduced significantly the decreases in tidal volume and minute ventilation. This level of vagotomy did not affect vasopressor and bradycardic effects of NPY. Blockade of NPY Y 1 receptors with an intravenous dose of 5 mg/kg of BMS 193885, reduced significantly the cardio-respiratory effects of NPY injection. Pre-treatment with BIIE 0246, NPY 2 receptor antagonist at a dose of 1–2.5 mg/kg was not effective in blocking the response to NPY. The results of this study indicate that NPY-evoked activation of NPY Y 1 receptors decreases both components of the breathing pattern, and this response is primarily mediated central to the cervical vagi. Bradycardia and hypertensive effect of NPY are attributed to the excitation of peripheral and central NPY Y 1 receptors and occur outside of the vagal pathways.

Cardio-respiratory effects of intravenous injection of somatostatin were investigated in anaesthetized, spontaneously breathing rats that were: (i) neurally intact and subsequently bilaterally vagotomized in the neck, or (ii) midcervically vagotomized with later vagotomized at the supranodosal level, or (iii) midcervically vagotomized and subjected to section of the carotid sinus nerves (CSNs). Intravenous injection of 100 μg/kg of somatostatin before and after midcervical vagotomy-induced immediate slowing down of the respiratory rate and decreased tidal volume, mean arterial blood pressure (MAP) and heart rate. Supranodose vagotomy did not abolish somatostatin-induced respiratory depression. CSNs section eliminated all respiratory effects of somatostatin challenge. In all the neural states, somatostatin caused significant falls in mean arterial blood pressure and heart rate. The results of this study suggest that hypoventilation induced by intravenous somatostatin administration occurs outside vagal afferentation to the medulla and is mediated via carotid body afferents. Sino-aortic chemoreceptors and baroreceptors do not contribute to bradycardia and a fall in blood pressure. These cardiovascular effects are presumably mediated due to excitation of somatostatin receptors within the heart and/or in the brain.

The respiratory effects evoked by systemic injection of bombesin were studied in spontaneously breathing rats that were (i) neurally intact and subsequently bilaterally vagotomized, (ii) intact, before and after pharmacological blockade of the bombesin BB(1) and BB(2) receptors. An intravenous bolus of bombesin (10 microg/kg) evoked sighs, decrease in the breathing rate, augmentation of tidal volume and an increase in mean arterial blood pressure. Midcervical vagotomy abolished all respiratory changes evoked by bombesin challenge, but did not prevent the increase in blood pressure. Blockade of BB(1) and BB(2) receptors with an intravenous dose of 50 microg/kg of [D-Phe](12)-bombesin, reduced significantly the cardio-respiratory effects due to bombesin administration. The BB(1) receptors antagonist, BIM 23127, at a dose of 100 microg/kg did not block the response to bombesin. These results indicate that bombesin given systemically stimulates ventilation by activation of BB(2) receptors affecting mainly the tidal component of the breathing pattern, and that the response is mediated by the lung vagi. The hypertensive effect of bombesin resulted from the excitation of BB(2) receptors, but occurred outside vagal afferentation from the lungs.

The respiratory effects resulting from stimulation of 5-HT(1A) receptors were studied in spontaneously breathing rats that were: (i) neurally intact and subsequently bilaterally vagotomized; (ii) subjected to bilateral midcervical vagotomy followed by supranodosal vagotomy; (iii) midcervically vagotomized and treated by carotid sinus/body denervation; or (iv) subjected to infra- and supranodosal vagotomy followed by pharmacological blockade of 5-HT(1A) receptors. An intravenous bolus of the 5-HT(1A) receptor agonist 8-hydroxy-dipropylaminotetralin (8-OH-DPAT, 10 microg kg(-1)) evoked increases in both breathing rate and tidal volume. After section of the midcervical and supranodosal vagi, 8-OH-DPAT challenge still increased the respiratory rate and tidal volume. Carotid sinus/body denervation did not reduce the augmentation of the tidal volume, but prevented the increase in breathing rate. Blockade of 5-HT(1A) receptors with intravenous doses of 1-(2-metoxyphenyl)-4-[4-(2-phthalimido) butyl] piperazine (NAN 190; 20 microg kg(-1)) abolished all respiratory effects of 8-OH-DPAT challenge. In all the neural states, 8-OH-DPAT evoked a significant fall in mean arterial blood pressure. Pretreatment with NAN 190 reduced baseline values of mean arterial pressure and prevented 8-OH-DPAT-induced hypotension. These results indicate that: (i) 8-OH-DPAT-evoked activation of 5-HT(1A) receptors increases breathing rate and tidal volume, which persists after section of the lung vagi and the nodose ganglia, but only the increase in breathing rate was abolished by carotid sinus/body denervation; and (ii) 8-OH-DPAT hyperventilatory and hypotensive responses result from the excitation of presumed 5-HT(1A) carotid receptors and the central 5-HT(1A)-expressing neurones.

The respiratory effects of stimulation of alpha2-adrenergic receptors were studied in spontaneously breathing anaesthetized rats that were neurally intact, or bilaterally vagotomized, or subjected to bilateral combined midcervical vagotomy and section of the carotid sinus nerves. An intravenous clonidine bolus (15 microg kg(-1)) evoked a prolonged slowing of the respiratory rate in all the neural states explored. Vagotomy reduced the early clonidine-evoked decline, but not the augmentation of tidal volume that followed the decline. After section of the carotid sinus nerves, clonidine challenge continued to decrease the respiratory rate, but not the tidal volume. Blockade of alpha2-adrenergic receptors with intravenous doses of SKF 86466 (200 microg kg(-1)) abolished all respiratory effects of the clonidine challenge. In all the neural states studied, clonidine evoked a significant short-lived rise in mean arterial blood pressure followed by a decrease below the respective prechallenge value. The SKF 86466 pretreatment lowered mean arterial blood pressure control values and reduced the magnitude of postclonidine changes. These results indicate that: (i) clonidine-evoked activation of alpha2-adrenergic receptors affects the two components of the breathing pattern differently, and this occurs beyond the lung vagi; and (ii) changes in tidal volume result from excitation of the carotid bodies and are coupled with centrally mediated slowing of the respiratory rhythm.

Respiratory effects of NMDA injection into the right atrium were investigated in 11 urethane-chloralose anaesthetised and spontaneously breathing rats. The animals were initially vagotomised and six of them were subdued to the subsequent carotid sinus nerve section, and the other five were treated by NMDA antagonist. Bolus injection of NMDA (27 micromol/kg) induced the depression of ventilation in all rats, due to the decrease in tidal volume from a baseline of 2.98 +/- 0.4 to 2.63 +/- 0.3 ml (P < 0.01), and slowing down of the respiratory rate from a baseline of 56 +/- 2.6 to 27 +/- 2.0 breaths min(-1) (P < 0.0001). Section of the carotid sinus nerves (CSNs) precluded the respiratory depression. Prolongation of the expiratory time was reduced by this neurotomy from 5.07 +/- 2.6 to 1.04 +/- 0.03 (P < 0.05). In five rats the blockade of NMDA receptors with the selective antagonist (AP-7) was likewise efficient in eliminating the post-NMDA respiratory response. NMDA increased mean arterial blood pressure and this rise occurred beyond the afferentation from the carotid bodies and the blockade of NMDA receptors. Results of this study indicate that inhibition of the respiratory drive evoked by NMDA administered via the peripheral circulation requires intact carotid bodies and activation of NMDA receptors.

1. Experiments were performed to determine the effects of systemic application of N-methyl-d-aspartate (NMDA) on respiratory variables and blood pressure in 22 urethane/chloralose-anaesthetized, spontaneously breathing rats. 2. Bolus injection of NMDA at a dose of 27 micro mol/kg, i.v., in neurally intact rats evoked a depression of breathing, most apparent at 30 s, comprising a decrease in tidal volume (P < 0.001) and respiratory rate (P < 0.001). The expiratory apnoea appeared in three intact rats only. 3. The respiratory effects of NMDA were independent of the vagal integrity between lungs and the nodose ganglia. Elimination of supranodose connection to the medulla reduced the prolongation of the expiratory time (P < 0.01). 4. N-Methyl-d-aspartate induced an initial rise in blood pressure followed by hypotension in rats treated by infra- and supranodose vagotomy. 5. It is concluded that the respiratory response to systemic NMDA challenge occurs beyond lung vagi and indicates that neurons of the nodose ganglia contribute to NMDA inhibition of the expiratory time.

Ile(9)PK20 is a novel hybrid of opioid-neurotensin peptides synthesized from the C-terminal hexapeptide of neurotensin and endomorphin-2 pharmacophore. This chimeric compound shows potent central and peripheral antinociceptive activity in experimental animals, however nothing is known about its influence on the respiratory and cardiovascular parameters. The present study was designed to determine the cardiorespiratory effects exerted by an intravenous injection (i.v.) of [Ile(9)]PK20. Share of the vagal afferentation and the contribution of NTS1 neurotensin and opioid receptors were tested. Intravenous injection of the hybrid at a dose of 100 μg/kg in the intact, anaesthetized rats provoked an increase in tidal volume preceded by a prompt short-lived decrease. Immediately after the end of injection brief acceleration of the respiratory rhythm appeared, and was ensued by the slowing down of breathing. Changes in respiration were concomitant with a bi-phasic response of the blood pressure: an immediate increase was followed by a sustained hypotension. Midcervical vagotomy eliminated the increase in tidal volume and respiratory rate responses. Antagonist of opioid receptors - naloxone hydrochloride eliminated only [Ile(9)]PK20-evoked decline in tidal volume response. Blockade of NTS1 receptors with an intravenous dose of SR 142,948, lessened the remaining cardiorespiratory effects. This study depicts that [Ile(9)]PK20 acting through neurotensin NTS1 receptors augments the tidal component of the breathing pattern and activates respiratory timing response through the vagal pathway. Blood pressure effects occur outside vagal afferentation and might result from activation of the central and peripheral vascular NTS1 receptors. In summary the respiratory effects of the hybrid appeared not to be profound, but they were accompanied with unfavourable prolonged hypotension.

The key role of the vagus nerves in the reflex control of breathing is generally accepted. Cardiopulmonary vagal receptors and their afferent connection with the medullary respiratory centers secures the proper regulatory feedback. Section of the vagi at the midcervical level interrupts primary vagal reflexes and those due to activation of lung afferents by neuroactive substances. In this context the present review focuses on the reflex contribution of the inferior (nodose) vagal ganglia to the respiratory pattern, considering that this structure contains perikarya of vagal afferent neurons which house neurotransmitters, neuropeptides and neurochemical substances. In experimental animals with removed sensory input from the lungs (midcervical vagotomy) the following evidence was reported. Transient respiratory suppression in the form of apnoea, occurring after systemic injection of serotonin, adenosine triphosphate and anandamide (N-arachidonoyl-ethanolamine-endogenous cannabinoid neurotransmitter), which was abrogated by nodose ganglionectomy. Preserved nodose-NTS connection conditioned respiratory depression affecting the timing component of the breathing pattern evoked by N-6-cyclopentyl-adenosine (CPA) and inhibition of both respiratory constituents induced by NPY. Stimulatory effect of NPY13-36 on tidal volume required nodosal connection. The cardiovascular effects of majority of the tested substances occurred beyond the nodose ganglia (with exclusion of serotonin and anandamide).

Majority of nosocomial Acinetobacter baumannii strains are highly resistant to many available groups of antibiotics, causing therapy of infections the clinical challenge. The aim of study was to estimate of resistance development to sulbactam, cefoperazone and cefoperazone/sulbactam in Acinetobacter baumannii clinical strains.Five Acinetobacter baumannii strains (Acb1, Acb2, Acb4, Acb13 and Acb25) were identified by the VITEK 2 GN card and the automatic system VITEK 2 according to the procedure and following the producer's instructions. Additionaly, the belonging of the strains to the species was confirmed by the presence of the bla(OXA-51-like) gene. Initial and after antibiotic exposure MIC values of sulbactam, cefoperazone and cefoperazone/sulbactam were determined by using a broth microdilution method. Antibiotic pressure of examined strains was performed in Mueller-Hinton broth containing 0,5x, 0,9x and 2x initial MIC of individual compounds during six-day passages and next six-day passages without antibiotic presence. The Mann-Whitney U test and Kruskal-Wallis non-prarametric Anova test were used to statistical analysis.Serial passaging of Acinetobacter baumannii strains in the presence of antibiotics caused permanent increasing MIC value independently of used concentrations in the majority of examined strains. The highest MIC value increase of sulbactam was found in Acb4 strain. Even after two passages this isolate changed MIC from 0.5 microg/ml to 4 microg/ml (increase about four levels of concentration). Moreover, after incubation in 0.9x MIC concentration similar observation was noted. No normalization of MIC value of sulbactam after incubation during next six passages without sulbactam was observed. In case of cefoperazone the highest levels of induction were noted in Acb1, Acb13 and Acb25 strains. In these strains, after two passages in presence of cefoperazone (2xMIC) the exceedance of minimal of growth concentration over the highest examined concentration was observed. Similar effects were observed in Acbl strain after stimulation with 0.9x and 0.5x MIC cefoperazone. Return of initial MIC values was received only after induction with 0.5 x MIC cefoperazone. In some cases, no opportunities for evaluation of resistance development was noted, because during stimulation with 2x MIC of used antibiotics concentarations, bactericidal effect was found.Sulbactam, cefoperazone and cefoperazone/sulbactam rapidly induce increasing of resistance in Acinetobacter baumannii clinical isolates. Statistically essential MIC increase after using higher concentration than lower was showed. This effect was particularly visible in the case of stimulation of cefoperazone/sulbactam combination.

The purpose of our study was to determine the cardio-respiratory pattern exerted by the systemic injection of neurotensin, contribution of neurotensin NTS(1) receptors and the neural pathways mediating the responses. The effects of an intravenous injection (i.v.) of neurotensin were investigated in anaesthetized, spontaneously breathing rats in following experimental schemes: (i) control animals before and after midcervical vagotomy; (ii) in three separate subgroups of rats: neurally intact, vagotomized at supranodosal level and initially midcervically vagotomized exposed to section of the carotid sinus nerves (CSNs); (iii) in the intact rats 2 minutes after blockade of neurotensin NTS(1) receptors with SR 142948. Intravenous injection of 10 μg/kg of neurotensin in the intact rats evoked prompt increase in the respiratory rate followed by a prolonged slowing down coupled with augmented tidal volume. Midcervical vagotomy precluded the effects of neurotensin on the frequency of breathing, while CSNs section reduced the increase in tidal volume. In all the neural states neurotensin caused significant fall in mean arterial blood pressure preceded by prompt hypertensive response. The cardio-respiratory effects of neurotensin were blocked by pre-treatment with NTS(1) receptor antagonist. The results of this study showed that neurotensin acting through NTS(1) receptors augments the tidal component of the breathing pattern in a large portion via carotid body afferentation whereas the respiratory timing response to neurotensin depends entirely on the intact midcervical vagi. Blood pressure effects evoked by an intravenous neurotensin occur outside vagal and CSNs pathways and might result from activation of the peripheral vascular NTS(1) receptors.

Extended spectrum β-lactamases production is one of the most common mechanism of resistance to extended spectrum β-lactam antibiotics is increasing worldwide. Twenty five strains of Klebsiella pneumoniae isolated from clinical specimens were tested. Based on the phenotypic confirmatory test all these strains were defined as ESBL producers named ESBL(+). The plasmid DNA from each strains was used to investigate the presence of blaSHV genes responsible for extended spectrum β-lactamases production. Moreover, susceptibility of these strains to antibiotic other than β-lactams in was tested.

The aim of the present study was to investigate the effects of aortic depressor nerve (ADN) transection, supranodosal vagi denervation (NG vagi cut) and adrenergic receptor blocker treatment on the cardiovascular responses evoked by systemic injection of bombesin. The cardiovascular effects were studied in spontaneously breathing rats that were (i) bilaterally, midcervically vagotomized (MC vagi cut) and subjected to section of the aortic depressor nerves, (ii) midcervically vagotomized and subsequently vagotomized at the supranodosal level or (iii) midcervically vagotomized before and after pharmacological blockade of α- or β-adrenergic receptors with phentolamine and propranolol, respectively. An intravenous bolus of bombesin (10 μg/kg) in midcervically vagotomized and ADN denervated animals increased mean arterial blood pressure (MAP) and heart rate (HR). An approximate 20% increase in blood pressure occurred immediately following bombesin injection and lasted for 2-3 min. Augmentation of the heart rate occurred 30-60 s after the bombesin challenge and persisted for more than 10 min. After section of the supranodosal vagi, bombesin failed to induce an increase in heart rate. Blockade of α-adrenergic receptors with an intravenous dose of phentolamine significantly reduced post-bombesin hypertension. These results indicate that bombesin-evoked increases in blood pressure do not require aortic depressor nerves and supranodosal vagi and are presumably mediated by the activation of peripheral α-adrenergic receptors. Bombesin-induced tachycardia was dependent on an intact supranodose pathway and was amplified by activation of β-adrenoceptors.

Staphylococcus aureus obtained from a University Hospital in Poland were characterized in relation to resistance to aminoglycoside antibiotics and the distribution of the genes encoding the most clinically relevant aminoglycoside modifying enzymes (AMEs). Of a total of 118 S. aureus, 45 (38.1%) isolates were found to be resistant to at least one of the tested antibiotics. All aminoglycoside resistant isolates except one 44 (97.8%) were resistant to kanamycin. The majority of strains 37 (82.2%) and 32 (71.1%) expressed resistance to neomycin and tobramycin, respectively. Eleven strains (24.4%) were resistant to gentamicin or amikacin. All S. aureus strains were sensitive to netilmicin. The most prevalent resistance gene was aac(6')-Ie+aph(2') found in 13 (28.9%) strains and 12 (26.7%) isolates carried ant(4')-Ia gene, whilst aph(3')-IIIa gene was detected in only 7 (15.6%) isolates. Additionally, the ant(6)-Ia and str genes were detected in 14 (31.1%) and 2 (4.4%) strains, respectively. Ten (22.2%) strains resistant to amikacin, tobramycin, kanamycin or neomycin did not harbor any of the above-noted genes.

The respiratory effects resulting from stimulation of 5-HT(1A) receptors were studied in spontaneously breathing rats that were: (i) neurally intact and subsequently bilaterally vagotomized; (ii) subjected to bilateral midcervical vagotomy followed by supranodosal vagotomy; (iii) midcervically vagotomized and treated by carotid sinus/body denervation; or (iv) subjected to infra- and supranodosal vagotomy followed by pharmacological blockade of 5-HT(1A) receptors. An intravenous bolus of the 5-HT(1A) receptor agonist 8-hydroxy-dipropylaminotetralin (8-OH-DPAT, 10 microg kg(-1)) evoked increases in both breathing rate and tidal volume. After section of the midcervical and supranodosal vagi, 8-OH-DPAT challenge still increased the respiratory rate and tidal volume. Carotid sinus/body denervation did not reduce the augmentation of the tidal volume, but prevented the increase in breathing rate. Blockade of 5-HT(1A) receptors with intravenous doses of 1-(2-metoxyphenyl)-4-[4-(2-phthalimido) butyl] piperazine (NAN 190; 20 microg kg(-1)) abolished all respiratory effects of 8-OH-DPAT challenge. In all the neural states, 8-OH-DPAT evoked a significant fall in mean arterial blood pressure. Pretreatment with NAN 190 reduced baseline values of mean arterial pressure and prevented 8-OH-DPAT-induced hypotension. These results indicate that: (i) 8-OH-DPAT-evoked activation of 5-HT(1A) receptors increases breathing rate and tidal volume, which persists after section of the lung vagi and the nodose ganglia, but only the increase in breathing rate was abolished by carotid sinus/body denervation; and (ii) 8-OH-DPAT hyperventilatory and hypotensive responses result from the excitation of presumed 5-HT(1A) carotid receptors and the central 5-HT(1A)-expressing neurones.

Respiratory effects of intracarotid injection of gamma-amino-butyric acid (GABA) were investigated in two groups of rats. In the first group of 12 rats the effects of GABA were checked in the intact state, following bilateral vagotomy and GABA receptor blockade. The second group consisted of five initially vagotomized rats, challenged with GABA prior to and after bilateral carotid chemodenervation (CSN-cut). All rats were urethane and chloralose anaesthetized and spontaneously breathing. Injection of 39 micromol/kg GABA prior to and after vagotomy induced an expiratory apnoea of, respectively 5.5+/-0.84 sec and 3.9+/-0.6 sec duration (mean+/-S.E.M.), P0.05 in all 12 rats. In breaths that followed the apnoea tidal volume increased above the control level by 23.3% (P0.01) and 25.6% (P0.01) pre- and post-vagotomy, respectively. Blockade of GABA receptors with bicuculline and picrotoxin abolished the inhibition of breathing. In five vagotomized rats with intact carotid sinus nerves (CSNs) intracarotid GABA challenge increased tidal volume by 39% compared with baseline breathing (P0.05). Section of the CSNs precluded the occurrence of apnoea and undergoing respiratory changes evoked by GABA. Intracarotid GABA caused significant decrease in the mean blood pressure independent of the neural state, but the fall was delayed by CSNs neurotomy. Results of this study indicate that GABA given systemically induces apnoea followed by post-apnoeic hyperventilation. Carotid bodies are required for the ventilatory response to GABA; vagal afferents are not involved in this response.

Respiratory effects of an intravenous injection of capsaicin were investigated in nine vagotomized and subsequently laryngeally deafferentated, urethane- and chloralose-anaesthetized and spontaneously breathing rats. Bolus injection of capsaicin (5 micrograms/kg) into the right femoral vein induced an expiratory apnoea of 4.23 +/- 0.63 s duration (mean +/- SEM). In post-apnoeic breathing, tidal volume increased by 14% from the control level (P0.05) in all nine rats treated by vagotomy. Section of the superior laryngeal nerves (SLNs) precluded the occurrence of apnoea. Results of this study indicate that in vagotomized rats sensory input from the larynx constitutes an important pathway to the nodose ganglia endowed with capsaicin receptors.