TEMPORAL CHANGES IN LEFT-VENTRICULAR FUNCTION AFTER MASSIVE SYMPATHETIC NERVOUS-SYSTEM ACTIVATION

Citation
Sa. Lang et al., TEMPORAL CHANGES IN LEFT-VENTRICULAR FUNCTION AFTER MASSIVE SYMPATHETIC NERVOUS-SYSTEM ACTIVATION, Canadian journal of physiology and pharmacology, 72(6), 1994, pp. 693-700
Citations number
31
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
00084212
Volume
72
Issue
6
Year of publication
1994
Pages
693 - 700
Database
ISI
SICI code
0008-4212(1994)72:6<693:TCILFA>2.0.ZU;2-D
Abstract
Intense activation of the sympathetic nervous system (SNS) decreases t he 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 mu g/kg) was injected intracisternally to activate the SNS in six chloralose-anesthetized d ogs, 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 c urves (stroke work versus LVEDP or stroke work versus LV transmural pr essure) showed a marked decrease in slope and a shift to the right wit hin minutes after activating the SNS, which persisted for the duration of the experiment. These data indicate that LV contractility was dimi nished in these animals. No changes in LV function were observed in th ree dogs serving as time-matched controls. In three additional dogs, L V pressure was raised to a degree similar to that observed after SNS a ctivation by constricting the ascending aorta for 1 h. These animals e xhibited 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, bu t only minor changes were observed in the other two groups. We conclud e that myocardial contractility declines markedly soon after massive S NS activation and is not solely a function of the initial hypertensive period.