Temporal changes in left ventricular function after massive sympathetic nervous system activation

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Abstract
Intense activation of the sympathetic nervous system (SNS) decreases the contractile state of the rabbit left ventricle (LV). In this study, we determined the time course of LV dysfunction after massive central activation of the SNS in dogs. Veratrine (40–80 μg/kg) was injected intracisternally to activate the SNS in six chloralose-anesthetized dogs, and LV end-diastolic pressure (LVEDP), cardiac output, heart rate, and aortic pressure (Pa) were measured at 30-min intervals for 3 h. Pa increased from 147 ± 8 (SE) to 272 ± 7 mmHg (1 mmHg = 133.3 Pa) within 15 min, then declined to 148 ± 16 mmHg by 1 h. LV function curves (stroke work versus LVEDP or stroke work versus LV transmural pressure) showed a marked decrease in slope and a shift to the right within minutes after activating the SNS, which persisted for the duration of the experiment. These data indicate that LV contractility was diminished in these animals. No changes in LV function were observed in three dogs serving as time-matched controls. In three additional dogs, LV pressure was raised to a degree similar to that observed after SNS activation by constricting the ascending aorta for 1 h. These animals exhibited only modest shifts in the LV function curve during and after aortic constriction. Mean plasma catecholamine concentration increased by one to two orders of magnitude in animals after SNS activation, but only minor changes were observed in the other two groups. We conclude that myocardial contractility declines markedly soon after massive SNS activation and is not solely a function of the initial hypertensive period.Key words: left ventricle contractility, heart failure, neurogenic pulmonary edema, sympathetic nervous system, catecholamines, veratrine.

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