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颈动脉窦压力感受性反射系统控制血管容量中的α和β肾上腺素能机制。

Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system.

作者信息

Shigemi K, Brunner M J, Shoukas A A

机构信息

Department of Biomedical Engineering, Johns Hopkins Medical School, Baltimore 21205.

出版信息

Am J Physiol. 1994 Jul;267(1 Pt 2):H201-10. doi: 10.1152/ajpheart.1994.267.1.H201.

Abstract

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

摘要

我们研究了α-和β-肾上腺素能受体机制对麻醉、迷走神经切断的犬类中颈动脉窦压力反射系统引起的全身血管容量变化的主动和被动贡献。将颈动脉窦与体循环隔离,并用控制压力进行灌注。为了确定血管容量的变化,使用了恒流、恒静脉压心肺旁路。当颈动脉窦压力从200 mmHg降至50 mmHg时,在未使用任何肾上腺素能受体拮抗剂、使用α-(酚妥拉明)或β-(普萘洛尔)拮抗剂以及同时使用两种拮抗剂的情况下,计算无应力血管容量的变化。全身循环中无应力血管容量的反射性变化(未使用任何拮抗剂时为22.6±9.0 ml/kg),使用酚妥拉明时降低了72%,使用普萘洛尔时降低了35%,同时使用两种拮抗剂时降低了73%。我们的结果表明,α-肾上腺素能机制对全身静脉容量的主动变化有显著贡献。此外,β-肾上腺素能系统对静脉血管的主动变化影响很小,但在颈动脉窦压力反射系统激活时,通过扩张肝流出阻力,对总体容量变化有贡献。

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