Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a small, but significant, increase in frequency during hypercapnia in vagotomized, anesthetized animals, indicating involvement of an extravagal mechanism in the response. The intent of this study was to determine the source of this second mechanism regulating frequency during hypercapnia. Experiments were performed on 22 vagotomized, anesthetized (Dial) cats. Frequency (f), inspiratory time (ti) and expiratory time (te) responses to CO2 were monitored before and after sectioning of afferent nerves from the carotid bodies (carotid sinus nerve section), chest wall (dorsal rhizotomies, T1-T12) and diaphragm (dorsal rhizotomies. C4-C7). Most vagotomized animals responded to 6% CO2 with an increased frequency, decreased ti and no consistent change in te. The responses to CO2 were essentially unaltered following chest wall and diaphragm deafferentation. Sodium cyanide stimulation of the carotid bodies produced similar respiratory pattern changes as CO2; furthermore, the f and ti changes with CO2 were still present following carotid body deafferentiation. The results of this study suggest that: (1) afferents from chest wall and diaphragm mechanoreceptors are not responsible for the vagal-like effects on ti and f during hypercapnia, (2) afferents from lung mechanoreceptors, via the vagus nerves, are the only inputs from respiratory mechanoreceptors causing an increased f during hypercapnia, (3) the extravagal mechanism responsible for the decreased ti and increased f during hypercapnia is inherent to the medullary-pontine rhythm generator, and (4) input from the chemoreceptors can elicit the response.
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PMID:Respiratory frequency control during hypercapnia in vagotomized, anesthetized cats. 97 52

N-methyl-D-aspartate (NMDA) glutamate receptors mediate critical components of cardiorespiratory control in anesthetized animals. The role of NMDA receptors in the ventilatory responses to peripheral and central chemoreceptor stimulation was investigated in conscious, freely behaving rats. Minute ventilation (VE) responses to 10% O2, 5% CO2, and increasing intravenous doses of sodium cyanide were measured in intact rats before and after intravenous administration of the NMDA receptor antagonist MK-801 (3 mg/kg). After MK-801, eupcapnic tidal volume (VT) decreased while frequency increased, resulting in a modest reduction in VE. Inspiratory time (TI) decreased, whereas expiratory time remained unchanged. The VE responses to hypercapnia were qualitatively similar in control and MK-801 conditions, with slight reductions in respiratory drive (VT/TI) after MK-801. In contrast, responses to hypoxia were markedly attenuated after MK-801 and were primarily due to reduced frequency changes, whereas VT was unaffected. Sodium cyanide doses associated with significant VE increases were 5 and 50 microg/kg before and after MK-801, respectively. Thus 1-log shift to the right of individual dose-response curves occurred with MK-801. Selective carotid body denervation reduced VE during hypoxia by 70%, and residual hypoxic ventilatory responses were abolished after MK-801. These findings suggest that, in conscious rats, carotid and other peripheral chemoreceptor-mediated hypoxic ventilatory responses are critically dependent on NMDA receptor activation and that NMDA receptor mechanisms are only modestly involved during hypercapnia.
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PMID:NMDA receptors mediate peripheral chemoreceptor afferent input in the conscious rat. 948 Sep 43