Lee R W, Standaert S, Lancaster L D, Buckley D, Goldman S
Department of Internal Medicine, Tucson Veterans Administration Medical Center, Arizona 85723.
J Clin Invest. 1988 Aug;82(2):413-9. doi: 10.1172/JCI113613.
To determine the cardiac and peripheral circulatory responses to changes in afterload with angiotension and vasopressin, we increased mean aortic pressure 25% and 50% above control in splenectomized and ganglion-blocked dogs. We compared these responses to similar mechanical increases in aortic pressure produced by partial balloon occlusion of the descending aorta. With 25% or 50% increases in aortic pressure, angiotensin, vasopressin, and balloon inflation produced no changes in heart rate, right atrial, and mean pulmonary artery pressures. At 25% increase in aortic pressure, cardiac output was maintained with angiotensin and balloon occlusion but decreased with vasopressin. At 50% increase in aortic pressure, cardiac output was maintained with only balloon occlusion and decreased with both angiotensin and vasopressin. Whenever cardiac output fell, central blood volume did not increase as after-load increased. These changes in preload can be explained by alterations in the venous circulation. Vasopressin did not alter venous compliance or unstressed vascular volume but increased resistance to venous return. Angiotensin also increased resistance to venous return but decreased venous compliance and did not change unstressed vascular volume. Balloon occlusion had no effects on these parameters. We conclude that: (a) angiotensin caused significant venoconstriction resulting in maintenance of cardiac output at 25% but not 50% increase in aortic pressure; (b) vasopressin increased the resistance to venous return without venoconstriction; this resulted in a fall in cardiac output even with a 25% increase in aortic pressure; and (c) the effects of the agents on the venous circulation were independent of the mechanical effects of a pressure increase in the arterial circulation.
为了确定血管紧张素和血管加压素引起后负荷变化时心脏和外周循环的反应,我们将脾切除和神经节阻断犬的平均主动脉压在对照值基础上提高25%和50%。我们将这些反应与降主动脉部分球囊闭塞引起的类似主动脉压机械性升高的反应进行比较。当主动脉压升高25%或50%时,血管紧张素、血管加压素和球囊充气对心率、右心房压和平均肺动脉压均无影响。主动脉压升高25%时,血管紧张素和球囊闭塞可维持心输出量,而血管加压素则使其降低。主动脉压升高50%时,只有球囊闭塞可维持心输出量,血管紧张素和血管加压素均使其降低。每当心输出量下降时,随着后负荷增加,中心血容量并未增加。这些前负荷的变化可通过静脉循环的改变来解释。血管加压素未改变静脉顺应性或无应力血管容量,但增加了静脉回流阻力。血管紧张素也增加了静脉回流阻力,但降低了静脉顺应性,且未改变无应力血管容量。球囊闭塞对这些参数无影响。我们得出以下结论:(a)血管紧张素引起显著的静脉收缩,从而在主动脉压升高25%而非50%时维持心输出量;(b)血管加压素增加静脉回流阻力但不引起静脉收缩;即使主动脉压升高25%,这也导致心输出量下降;(c)这些药物对静脉循环的影响独立于动脉循环压力升高的机械效应。