Why the study?
Does capsaicin injection into the pulmonary circulation cause reflex bronchoconstriction in dogs?
Does capsaicin injection into the pulmonary circulation cause reflex bronchoconstriction in dogs?
Capsaicin stimulates pulmonary receptors accessible via the pulmonary circulation to produce reflex bronchoconstriction mediated by the vagus nerve.
Answers are grounded in this paper and cite their sources.
Animal data indicate vagally mediated pulmonary chemoreflex bronchoconstriction in dogs; leaves open translation to human cardiopulmonary reflexes.
To determine whether receptors stimulated by the injection of capsaicin into the pulmonary circulation cause reflex changes in airway size, six dogs were anesthetized with chloralose, paralyzed with succinylcholine, and mechanically ventilated (2 cm H2O PEEP). Intrapulmonary airways were outlined with tantalum dust, and diameters were determined by taking serial roentgenograms at end expiration. Capsaicin (20 micrograms/kg) injected into the right ventricle significantly decreased airway diameter (20%), heart rate, aortic pressure, and pulmonary artery pressure. In contrast, capsaicin injected into the left ventricle did not alter airway diameter or aortic pressure, although heart rate and pulmonary artery pressure decreased but to a lesser extent than after right ventricular injection. After vagotomy, capsaicin had no effect on airway diameter or heart rate but aortic pressure and pulmonary artery pressure increased slightly. Results suggest that pulmonary receptors sensitive to capsaicin and accessible via the pulmonary circulation produce reflex bronchoconstriction. One possible function of this vagal reflex is to assist fluid movement from microvasculature to peribronchial space by reducing peribronchial pressure.
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Russell et al. (1979) studied this question.
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