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EN
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 g/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 (P<0.05) 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.
EN
The effects of an intravenous capsaicin challenge on the respiratory pattern and ventilation were studied in 15 urethane/chloralose-anaesthetized, spontanously breathing rats. Bolus injection of capsaicin at a dose of 5 mug/kg into the right femoral vein evoked respiratory arrest in all animals (both prior to and after bilateral midcervical vagotomy), which effect was abolished by ruthenium red pretreatment. Breathing that followed the apnoea was of enlarged tidal volume and initially increased respiratory rate, which resulted in an augmented ventilation. The capsaicin-induced respiratory changes were independent of vagal integrity and may depend on stimulation of vanilloid receptors within the nodose ganglia.
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EN
The pulmonary chemoreflex induced by an intravenous injection of serotonin (5-hydroxytryptamine) in cats consists of prompt apnoea, bradycardia and hypotension, followed by rapid, shallow breathing. The present study had two purposes (1) to compare the effect of 5HT on ventilation and laryngeal resistance in cats and (2) to assess the role of laryngeal afferents in these responses. The effects of an intravenous injection of serotonin at a dose of 0.05 mg per kg of body weight were studied in eighteen anaesthetized cats, breathing spontaneously via a tracheal cannula. In eleven cats the larynx was isolated in situ to measure laryngeal resistance. In post-serotonin apnoea, the expiratory laryngeal resistance rose four-fold. This coincided with the increased afferent activity of the superior laryngeal nerve. In the initial phase of resumed shallow breathing, the increase in the expiratory laryngeal resistance was coupled with reduced tidal volume. Bilateral section of the superior laryngeal nerve failed to affect laryngeal constriction and the ventilatory response to serotonin. Thus laryngeal afferents running within the superior laryngeal nerve are not essential for the respiratory phenomena induced by serotonin.
EN
Administration of serotonin (5-HT) to pulmonary circulation elicits prompt apnoea, followed by subsequent tachypnoea. The present study was designed to ascertain whether 5-HT challenge into the laryngeal artery will evoke the full constellation of this chemoreflex and to examine the role of laryngeal sensory input and importance of vagal afferents in the respiratory sequelae.The experiments were done on 10 anaesthetized, spontaneously breathing cats.Laryngeal artery injections of 5-HT, similarly to intravenous challenge, caused apnoeas, which were significantly diminished by the section of cervical vagal trunks. Breathing frequency increased in all condtions on intravenous injection but only prior to vagotomy, when administered into laryngeal artery. With resumed breathing,the peak inspiratory airflows were significantly increased in the neurally intact, those treated by bilateral section of the superior laryngeal nerves (SLNs-cut) and vagotomized cats, with no difference between them and independent of the route of injection. The results show that serotonin chemoreflex could evolve from the laryngeal vascular bed and that laryngeal afferents do not contribute to the respiratory arrest.
EN
Respiratory effects of an intra-common carotid artery injection of N-methyl-D-aspartic acid (NMDA) were investigated in anesthetized spontaneously breathing rats, using three experimental paradigms: (1) midcervical vagotomy followed by supranodosal vagotomy, (2) midcervical vagotomy followed by section of the carotid sinus nerves (CSNs), and (3) midcervical vagotomy followed by pharmacological blockade of NMDA receptors. The intra-common carotid artery injection of NMDA (4 mg/kg) induced transient expiratory apnea followed by a brief and variably occurring period of breathing at reduced tidal volume. There were no consistent changes in respiratory rate in rats subjected to midcervical vagotomy alone. Supranodose vagotomy exerted no effect on NMDA-induced respiratory arrest, whereas CSNs' section or blockade of NMDA receptors with AP-7 abolished the apnea. These results indicate that the apnea induced by intra-arterial NMDA challenge is due to activation of peripheral NMDA receptors and is mediated via carotid body afferents.
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