Cardiorespiratory reflex due to pulmonary J receptors stimulation by acetaldehyde in rats

• Published in: Alcohol (Fayetteville, N.Y.) Vol. 9; no. 4; p. 317
• Main Authors: Brugère, S S, Penna, M A, Corrales, R J
• Format: Journal Article
• Language: English
• Published: United States 01.07.1992
• Subjects: Acetaldehyde - pharmacology; Animals; Apnea - chemically induced; Bradycardia - chemically induced; Female; Heart - drug effects; Heart - physiology; Hypotension - chemically induced; Lung - drug effects; Lung - physiopathology; Male; Rats; Reflex; Respiration - drug effects; Respiration - physiology; Sensory Receptor Cells - drug effects; Sensory Receptor Cells - physiology
• ISSN: 0741-8329
• DOI: 10.1016/0741-8329(92)90073-J

Acetaldehyde (AcH) administered intravenously or into the right ventricle induces reflex bradycardia, hypotension, and apnea in the rat. The efferent pathway for this reflex is vagal and probably secondary to pulmonary J receptors stimulation. Located between the alveoli and the pulmonary capillary, J receptors are accessible through the pulmonary circulation and the airways. For this reason, a method for indirect nebulization (IN) of AcH into the airways, that provides a continuous record of respiration without changes in intrapulmonary pressure, was developed. IN of AcH (n = 14) induced bradycardia (64 +/- 3.1%), hypotension (34 +/- 4.2%), and apnea (79%), which were blocked by vagotomy (n = 9). The latencies (s) for bradycardia (0.34 +/- 0.06), hypotension (0.68 +/- 0.11), and apnea (0.25 +/- 0.11) were significantly shorter than those obtained by the intravenous route. Three rats that did not develop apnea had an equivalent response, where both tidal volume and minute ventilation decreased about 40% and these effects were also blocked by vagotomy. Indirect nebulization of AcH allowed us to demonstrate that pulmonary J receptors are responsible for this reflex response.