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动态运动开始时血管传导率的快速上升是由于肌肉泵的作用吗?

Is rapid rise in vascular conductance at onset of dynamic exercise due to muscle pump?

作者信息

Sheriff D D, Rowell L B, Scher A M

机构信息

Department of Physiology and Biophysics, School of Medicine, University of Washington, Seattle 98195.

出版信息

Am J Physiol. 1993 Oct;265(4 Pt 2):H1227-34. doi: 10.1152/ajpheart.1993.265.4.H1227.

DOI:10.1152/ajpheart.1993.265.4.H1227
PMID:8238409
Abstract

We tested the hypothesis that rapid increases in muscle blood flow and vascular conductance (C) at onset of dynamic exercise are caused by the muscle pump. We measured arterial (AP) and central venous pressure (CVP) in nine awake dogs, eight with atrioventricular block, pacemakers, and ascending aortic flow probes for control of cardiac output (CO) (2 also had terminal aortic flow probes). One dog had only an iliac artery probe. At exercise onset (0 and 10% grade, 4 mph) C and CVP rose to early plateaus, and AP reached a nadir, all in 2-5 s. At 20% grade and 4 mph, C increased continuously after its initial sudden rise. Timing and magnitude of initial change in conductance (delta C) were independent of CO, AP, work rate (change in grade at constant speed), or autonomic function (blocked by hexamethonium). Speed of initial delta C and its independence from work rate and blood flow ruled out metabolic vasodilation as its cause; insensitivity to AP and autonomic blockade ruled out myogenic relaxation and sympathetic vasodilation as causes of sudden delta C. Sensitivity to contraction frequency (not work per se) implicates the muscle pump. When reflexes were blocked, a large secondary rise in C, presumably caused by metabolic vasodilation, began after 10 s of mild exercise. When reflexes were intact in mild exercise, C was lowered below its initial plateau by sympathetic vasoconstriction, which partially raised AP from its nadir toward its preexercise level. Our conclusion is that dynamic exercise has a large rapid effect on C that is not explained by known neural, metabolic, myogenic, or hydrostatic influences.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们检验了这样一个假设

动态运动开始时肌肉血流量和血管传导率(C)的快速增加是由肌肉泵引起的。我们在9只清醒的狗身上测量了动脉压(AP)和中心静脉压(CVP),其中8只狗有房室传导阻滞、起搏器以及用于控制心输出量(CO)的升主动脉血流探头(2只还装有终末主动脉血流探头)。1只狗仅装有髂动脉探头。在运动开始时(坡度为0和10%,速度为4英里/小时),C和CVP在2 - 5秒内升至早期平台期,而AP降至最低点。在坡度为20%、速度为4英里/小时时,C在最初突然升高后持续增加。传导率初始变化(ΔC)的时间和幅度与CO、AP、工作速率(恒定速度下坡度的变化)或自主神经功能(被六甲铵阻断)无关。初始ΔC的速度及其与工作速率和血流的独立性排除了代谢性血管舒张是其原因;对AP和自主神经阻滞不敏感排除了肌源性舒张和交感神经血管舒张是ΔC突然变化的原因。对收缩频率(而非本身的工作)敏感表明是肌肉泵所致。当反射被阻断时,在轻度运动10秒后,C会出现大幅继发性升高,推测是由代谢性血管舒张引起的。当在轻度运动中反射完整时,C会因交感神经血管收缩而降至初始平台期以下,这会使AP从最低点部分回升至运动前水平。我们的结论是,动态运动对C有快速且显著的影响,这无法用已知的神经、代谢、肌源性或流体静力影响来解释。(摘要截断于250字)

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