| Literature DB >> 2749028 |
M I Hersch1, J G McLeod, P M Satchell, R G Early, C E Sullivan.
Abstract
Slowly adapting pulmonary stretch receptors (SARs) participate in numerous respiratory reflexes, including the Hering-Breuer lung inflation reflex (HBR), and reflex control of respiratory rate and depth. In addition, SAR discharge may modulate airway tone. We studied the effect of acrylamide neuropathy, which causes reversible dysfunction of SARs and their myelinated vagal afferents, on the breathing pattern, HBR and airway tone in conscious dogs. As neuropathy evolved, breathing became slow and deep, and both the apnoeic and bronchodilatory responses to lung inflation were markedly reduced, findings consistent with SAR dysfunction. Recovery of clinical neuropathy and respiratory reflexes followed acrylamide withdrawal. Despite the obvious abnormalities of SAR-mediated reflexes in acrylamide-affected dogs, airway tone remained normal and sinus arrhythmia prominent in the presence of neuropathy, suggesting that small diameter vagomotor efferents are relatively resistant to acrylamide. Acrylamide neuropathy provides a useful preparation for the study of vagomotor function in animals in which feedback from myelinated pulmonary afferents is attenuated.Entities:
Mesh:
Substances:
Year: 1989 PMID: 2749028 DOI: 10.1016/0034-5687(89)90102-3
Source DB: PubMed Journal: Respir Physiol ISSN: 0034-5687