HEMODYNAMIC AND NOREPINEPHRINE RESPONSES TO PACING-INDUCED HEART-FAILURE IN CONSCIOUS SINOAORTIC-DENERVATED DOGS

The present study was undertaken to determine the effects of chronic s inoaortic (baroreceptor) denervation (SAD) on the hemodynamic and symp athetic alterations that occur in the pacing-induced model of congesti ve heart failure. Two groups of dogs were examined: intact (n = 9) and SAD (n = 9). Both groups of dogs were studied in the control (prepace ) state and each week after the initiation of ventricular pacing at 25 0 beats/min. After the pacemaker was turned off, hemodynamic and plasm a norepinephrine levels returned toward control levels in the prepaced state and after 1 and 2 wk of pacing. However, by 3 wk all hemodynami c and norepinephrine levels remained relatively constant over the 10-m in observation period with the pacemaker off. With the pacemaker off, left ventricular end-diastolic pressure went from 2.7 +/- 1.4 (SE) mmH g during the prepace state to 23.2 +/- 2.9 mmHg in the heart failure s tate in intact dogs (P < 0.01). Left ventricular end-diastolic pressur e increased to 27.1 +/- 2.2 mmHg from a control level of 4.2 +/- 1.9 m mHg in SAD dogs (P < 0.0003). Mean arterial pressure significantly dec reased in intact and SAD dogs. Resting heart rate was significantly hi gher in SAD dogs and increased to 135.8 +/- 8.9 beats/min in intact do gs and 136.1 +/- 6.5 beats/min in SAD dogs. There were no significant differences in the hemodynamic parameters between intact and SAD dogs after pacing. Plasma norepinephrine was significantly lower in intact than in SAD dogs before pacing (197.7 +/- 21.6 vs. 320.6 +/- 26.6 pg/m l; P < 0.005). In the heart failure state, plasma norepinephrine incre ased significantly in both intact (598.3 +/- 44.2 pg/ml) and SAD (644. 0 +/- 64.6 pg/ml) groups. There were no differences in the severity or the magnitude of the developed heart failure state in SAD vs. intact dogs. We conclude from these data that the arterial baroreflex is not the sole mechanism for the increase in sympathetic drive in heart fail ure.