Effects of ischemia on cardiac afferent sympathetic and vagal reflexes in dog

To determine the time course of afferent sympathetic and vagal denervation after coronary occlusion and that of neural recovery after reperfusion, we measured the vasopressor responses to bradykinin and the vasodepressor responses to nicotine applied in a felt pad to the left ventricular epicardium of open-chest dogs. Shortly after latex injection of a diagonal branch of the left anterior descending coronary artery (LAD), the vasopressor response to bradykinin applied to the transmural ischemic area (n = 7) or apically to it (n = 6) was interrupted or attenuated. In contrast, nontransmural ischemia produced by ligation of the diagonal branch did not attenuate the response to bradykinin applied to the ischemic region (n = 6) or apically to it (n = 7). Transmural ischemia produced by occlusion of a diagonal branch of the LAD and a lateral marginal branch of the left circumflex coronary artery (n = 8) or by intraluminal balloon occlusion of the LAD (n = 7) decreased the vasopressor response to bradykinin applied within or apically to the ischemic area in less than 13 min. The vasopressor response to bradykinin became attenuated when the myocardial blood flow in the epicardial test site decreased to approximately 40% or less of the control value. Nontransmural ischemia produced by occlusion of a diagonal branch (n = 7) attenuated the vasodepressor response to nicotine applied to the nonischemic area apically to the occlusion in less than 13 min. A 15-min coronary occlusion followed by reperfusion produced reversible attenuation of afferent neural responses. We conclude that ischemia interrupts afferent sympathetic and vagal cardiac reflex responses to bradykinin and nicotine and that these alterations are reversible after reperfusion.