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在血管收缩剂诱导的高血压期间,通过自身调节血管收缩作用被放大。

Vasoconstriction is amplified by autoregulation during vasoconstrictor-induced hypertension.

作者信息

Meininger G A, Trzeciakowski J P

机构信息

Microcirculation Research Institute, College of Medicine, Texas A&M University, College Station 77843.

出版信息

Am J Physiol. 1988 Apr;254(4 Pt 2):H709-18. doi: 10.1152/ajpheart.1988.254.4.H709.

Abstract

This study investigated the degree to which autoregulation of blood flow interacts with vasoconstrictors to determine vascular resistance. Anesthetized rats were instrumented with a Doppler flow probe on the superior mesenteric artery (SMA) to measure blood flow and for calculation of vascular resistance. An adjustable occluder was placed on the SMA to set local perfusion pressure at values independent of mean arterial pressure (MAP) even when MAP was increased by the vasoconstrictors. Infusion of angiotensin II (ANG II, 50-1,247 ng.kg-1.min-1) produced a dose-dependent rightward shift in the intestinal pressure-flow relationship and elevated MAP from 85 to 127 mmHg. Low doses of phenylephrine (PE, 2.5-12.4 micrograms.kg-1.min-1) failed to shift the pressure-flow curve but did increase arterial pressure from 83 to 102 mmHg. At higher doses (25-62 micrograms.kg-1.min-1), PE also shifted the pressure-flow curve to the right. Maintaining local perfusion pressure at different values during the infusion of ANG II or PE produced a family of dose-response curves, with each exhibiting a different maximum change in resistance. When local pressure was permitted to increase with MAP, the composite dose-response curve for resistance that was obtained reflected the influence of the rise in local pressure (i.e., auto-regulation) and vasoconstrictor dose. At low doses of PE the increase in vascular resistance was attributable solely to an autoregulatory response related to the rise in MAP and not due to the constrictor effects of PE. Thus these data indicate that the rise in MAP accompanying systemic infusion of a vasoconstrictor stimulates autoregulation to amplify the local increase in vascular resistance.

摘要

本研究调查了血流的自动调节与血管收缩剂相互作用以确定血管阻力的程度。对麻醉大鼠的肠系膜上动脉(SMA)安装多普勒血流探头,以测量血流并计算血管阻力。在SMA上放置一个可调节的封堵器,以便将局部灌注压力设定为与平均动脉压(MAP)无关的值,即使MAP因血管收缩剂而升高时也是如此。输注血管紧张素II(ANG II,50 - 1247 ng·kg⁻¹·min⁻¹)使肠道压力 - 血流关系呈剂量依赖性向右移位,并使MAP从85 mmHg升高至127 mmHg。低剂量的去氧肾上腺素(PE,2.5 - 12.4 μg·kg⁻¹·min⁻¹)未能使压力 - 血流曲线移位,但确实使动脉压从83 mmHg升高至102 mmHg。在较高剂量(25 - 62 μg·kg⁻¹·min⁻¹)时,PE也使压力 - 血流曲线向右移位。在输注ANG II或PE期间将局部灌注压力维持在不同值会产生一系列剂量 - 反应曲线,每条曲线都表现出不同的最大阻力变化。当局部压力随MAP升高时,所获得的阻力复合剂量 - 反应曲线反映了局部压力升高(即自动调节)和血管收缩剂剂量的影响。在低剂量的PE时,血管阻力的增加仅归因于与MAP升高相关的自动调节反应,而不是由于PE的收缩作用。因此,这些数据表明,全身输注血管收缩剂时伴随的MAP升高会刺激自动调节,以放大局部血管阻力的增加。

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