Baro- and ventricular reflexes in conscious dogs subjected to chronic tachycardia

It has been well documented that the arterial baroreflex is depressed in chronic congestive heart failure. Furthermore, cardiopulmonary reflexes have also been shown to be depressed in heart failure. Because cardiac reflexes can be mediated by both mechanical and chemical stimuli, we undertook the current study to determine whether chemically activated cardiac reflexes (Bezold-Jarisch) are abnormally depressed in dogs with chronic heart failure at a point in time when arterial baroreflexes were clearly depressed. We studied heart rate and arterial pressure responses in 13 conscious instrumented dogs before and after chronic ventricular pacing at 250 beats/min for 4-5 wk. At the time the study was done each dog showed both hemodynamic and clinical signs of congestive heart failure. The arterial baroreflex was evaluated by analyzing the heart rate response to acute injections of phenylephrine and nitroglycerin. The Bezold-Jarisch reflex was assessed in nine dogs by determining the heart rate and blood pressure responses to intracoronary injections of various doses of veratridine. Arterial baroreflex responses were uniformly depressed following ventricular pacing. The phenylephrine slope was reduced by 55.8 ± 6.9% (P < 0.001), and the nitroglycerin slope was reduced by 67.9 ± 5.0% (P < 0.0001) in the heart failure state. Significant bradycardia and hypotension were seen at each dose of veratridine given (0.01, 0.1, and 0.4 μg/kg). When compared with the prepaced control state, the magnitude of the hypotension was no different in the heart failure state in response to any dose of veratridine. These data clearly indicate that while the arterial baroreflex control of heart rate is depressed in low-output heart failure, the bradycardia and hypotension in response to chemical stimulation of cardiac afferents is preserved. This finding suggests that baroreflex abnormalities may be related to afferent dysfunction rather than to a central or efferent abnormality.