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α1肾上腺素能对完整犬静脉循环的调控

Alpha-1 adrenergic control of the venous circulation in intact dogs.

作者信息

Appleton C, Olajos M, Morkin E, Goldman S

出版信息

J Pharmacol Exp Ther. 1985 Jun;233(3):729-34.

PMID:2861278
Abstract

To study alpha adrenergic control of the venous circulation, 17 dogs were lightly sedated and instrumented with thermodilution pulmonary flow and aortic catheters. Hemodynamics, cardiac output and central blood volume were measured at rest. Mean circulatory filling pressure, pressure gradient for venous return and resistance to venous return were calculated from pressures obtained during transient acetylcholine-induced circulatory arrest. Phenylephrine was then infused at two steady-state levels to increase mean aortic pressure by 50 and 100% above control values. Heart rate was controlled with atropine. Phenylephrine increased (P less than .025) mean aortic pressure from 80.7 +/- 2.9 to 121.3 +/- 7.6 to 164.7 +/- 6.1 mm Hg and systemic vascular resistance from 23.3 +/- 2.0 to 32.2 +/- 3.5 to 43.5 +/- 4.1 mm Hg/min/ml and did not change cardiac output (161.9 +/- 12.6-175.6 +/- 13.8-169.6 +/- 11.9 ml/min/kg). Mean circulatory filling pressure increased from 7.1 +/- 0.5 to 9.7 +/- 0.6 to 13.2 +/- 1.3 mm Hg (P less than .025). Pressure gradient for venous return increased from 6.4 +/- 0.4 to 7.7 +/- 0.4 to 8.9 +/- 0.4 mm Hg (P less than .025). Central blood volume increased from 16.2 +/- 0.9 to 19.4 +/- 1.4 to 22.0 +/- 1.9 ml/kg (P less than .025). To eliminate reflex changes in vascular tone, eight dogs received ganglionic blockade with trimethaphan. After ganglionic blockade phenylephrine increased cardiac output, systemic vascular resistance, mean circulatory filling pressure, pressure gradient for venous return and central blood volume (P less than .025). Thus, in conscious dogs, phenylephrine reduces peripheral vascular capacitance and shifts blood from the venous circulation to the central and arterial vascular compartments.

摘要

为研究静脉循环的α肾上腺素能控制,对17只狗进行轻度镇静,并安装热稀释肺动脉血流导管和主动脉导管。在静息状态下测量血流动力学、心输出量和中心血容量。根据短暂乙酰胆碱诱导的循环骤停期间获得的压力计算平均循环充盈压、静脉回流压力梯度和静脉回流阻力。然后以两个稳态水平输注去氧肾上腺素,使平均主动脉压比对照值升高50%和100%。用阿托品控制心率。去氧肾上腺素使平均主动脉压从80.7±2.9升高至121.3±7.6再至164.7±6.1 mmHg,全身血管阻力从23.3±2.0升高至32.2±3.5再至43.5±4.1 mmHg/min/ml,而心输出量不变(161.9±12.6 - 175.6±13.8 - 169.6±11.9 ml/min/kg)。平均循环充盈压从7.1±0.5升高至9.7±0.6再至13.2±1.3 mmHg(P<0.025)。静脉回流压力梯度从6.4±0.4升高至7.7±0.4再至8.9±0.4 mmHg(P<0.025)。中心血容量从16.2±0.9升高至19.4±1.4再至22.0±1.9 ml/kg(P<0.025)。为消除血管张力的反射性变化,8只狗接受了三甲噻芬的神经节阻滞。神经节阻滞后,去氧肾上腺素增加了心输出量、全身血管阻力、平均循环充盈压、静脉回流压力梯度和中心血容量(P<0.025)。因此,在清醒的狗中,去氧肾上腺素降低外周血管容量,并使血液从静脉循环转移至中心和动脉血管腔室。

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