Greene A S, Shoukas A A
Am J Physiol. 1986 Aug;251(2 Pt 2):H288-96. doi: 10.1152/ajpheart.1986.251.2.H288.
Venous return curves and cardiac function relationships were simultaneously determined in 10 pentobarbital-anesthetized dogs at three different isolated carotid sinus pressures. Changing carotid sinus pressure (CSP) between 50 and 200 mmHg produced large changes in the zero flow intercept of the venous return curves from 15.37 +/- 0.97 to 11.94 +/- 1.36 mmHg (P less than 0.001) but no change in slope. These changes in the intercept of the venous return curve were due to alterations in systemic vascular capacity caused by the carotid sinus baroreceptor reflex. Changes in the cardiac function curve with baroreceptor pressure were masked by concomitant changes in arterial pressure afterload; however, when arterial pressure was controlled, there was a significant change in the slope of the cardiac function curve from 60.32 +/- 26.9 to 37.06 +/- 13.31 ml X min-1 X kg-1 X mmHg-1 as CSP was changed from 50 to 200 mmHg. We conclude that changes in vascular capacity are the primary mechanism responsible for changes in cardiac output during activation of the carotid sinus baroreflex.
在10只戊巴比妥麻醉的犬中,于三种不同的孤立颈动脉窦压力下,同时测定静脉回流曲线与心功能的关系。将颈动脉窦压力(CSP)在50至200 mmHg之间变化时,静脉回流曲线的零流量截距发生了很大变化,从15.37±0.97 mmHg变为11.94±1.36 mmHg(P<0.001),但斜率未变。静脉回流曲线截距的这些变化是由颈动脉窦压力感受器反射引起的全身血管容量改变所致。压力感受器压力引起的心功能曲线变化被动脉压力后负荷的伴随变化所掩盖;然而,当控制动脉压力时,随着CSP从50 mmHg变为200 mmHg,心功能曲线的斜率从60.32±26.9变为37.06±13.31 ml·min-1·kg-1·mmHg-1,有显著变化。我们得出结论,血管容量的变化是颈动脉窦压力反射激活期间心输出量变化的主要机制。