Increased afferent vagal responses produced by epicardial application of nicotine on the canine posterior left ventricle.

Vagally mediated vasodepressor reflexes are observed in dogs and patients with acute myocardial ischemia or infarction and may be related to the Bezold-Jarisch reflex. To test whether nicotine and bradykinin produced site-specific vagal vasodepressor and sympathetic vasopressor responses, respectively, we compared blood pressure and heart rate responses to these drugs applied topically at six epicardial sites of the canine left ventricle: midanterior, apical anterior, midlateral, apical lateral, midposterior, and apical posterior left ventricle. In alpha-chloralose-anesthetized dogs with open chests a felt pad soaked in bradykinin (25 micrograms) or nicotine (50 micrograms) was applied to the test sites. Previous studies indicated that epicardial application of these drugs elicited a sympathetically mediated pressor response and a vagally mediated depressor response, respectively. Vasopressor response to bradykinin did not differ among six test sites in 10 dogs. However, vasodepressor response to nicotine was greater in the midposterior left ventricular epicardium than at other test sites in 16 dogs. A hypertensive response after the initial hypotensive response to nicotine was observed in the midanterior left ventricle and not in any other site. These data indicate that vagal vasodepressor responses to epicardial nicotine are greater in the canine midposterior left ventricle and are compatible with the higher incidence of bradycardia or hypotension during acute inferoposterior myocardial infarction in patients. Sympathetic vasopressor responses to epicardial bradykinin are not site specific. Half of the dogs showed no response to bradykinin or nicotine.