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运动时的心血管调节:血液动力学与机制

Cardiovascular adjustments to exercise: hemodynamics and mechanisms.

作者信息

Vatner S F, Pagani M

出版信息

Prog Cardiovasc Dis. 1976 Sep-Oct;19(2):91-108. doi: 10.1016/0033-0620(76)90018-9.

Abstract

The integrated response to severe exercise involves fourfold to fivefold increases in cardiac output, which are due primarily to increases in cardiac rate and to a lesser extent to augmentation of stroke volume. The increase in stroke volume is partly due to an increase in end-diastolic cardiac size (Frank-Starling mechanism) and secondarily due to a reduction in end-systolic cardiac size. The full role of the Frank-Starling mechanism is masked by the concomitant tachycardia. The reduction in end-systolic dimensions can be related to increased contractility, mediated by beta adrenergic stimulation. Beta adrenergic blockade prevents the inotropic response, the decrease in end-systolic dimensions, and approximately 50% of the tachycardia of exercise. The enhanced cardiac output is distributed preferentially to the exercising muscles including the heart. Blood flow to the heart increases fourfold to fivefold as well, mainly reflecting the augmented metabolic requirements of the myocardium due to near maximal increases in cardiac rate and contractility. Blood flow to the inactive viscera (e.g., kidney and gastrointestinal tract) is maintained during severe exercise in the normal dog. It is suggested that local autoregulatory mechanisms are responsible for maintained visceral flow in the face of neural and hormonal autonomic drive, which acts to constrict renal and mesenteric vessels and to reduce blood flow. However, in the presence of circulatory impairment, where oxygen delivery to the exercising muscles is impaired as occurs to complete heart block where normal heart rate increases during exercise are prevented, or in congestive right heart failure, where normal stroke volume increases during exercise are impaired, or in the presence of severe anemia, where oxygen-carrying capacity of the blood is limited, visceral blood flows are reduced drastically and blood is diverted to the exercising musculature. Thus,, visceral flow is normally maintained during severe exercise as long as all other compensatory mechanisms remain intact. However, when any other compensatory mechanism is disrupted (even the elimination of splenic reserve in the dog), reduction and diversion of visceral flow occur.

摘要

对剧烈运动的综合反应涉及心输出量增加四到五倍,这主要归因于心率的增加,在较小程度上也归因于每搏输出量的增加。每搏输出量的增加部分是由于舒张末期心脏大小的增加(弗兰克 - 斯塔林机制),其次是由于收缩末期心脏大小的减小。由于同时存在的心动过速,弗兰克 - 斯塔林机制的全部作用被掩盖。收缩末期尺寸的减小可能与β肾上腺素能刺激介导的收缩力增加有关。β肾上腺素能阻滞剂可防止变力反应、收缩末期尺寸的减小以及运动时约50%的心动过速。增强的心输出量优先分配到包括心脏在内的运动肌肉。流向心脏的血流量也增加四到五倍,这主要反映了由于心率和收缩力几乎最大程度增加导致心肌代谢需求增加。在正常犬剧烈运动期间,流向非活动内脏(如肾脏和胃肠道)的血流量得以维持。有人认为,在神经和激素自主驱动作用下,局部自动调节机制负责维持内脏血流,神经和激素自主驱动会使肾和肠系膜血管收缩并减少血流量。然而,在存在循环障碍的情况下,如发生完全性心脏传导阻滞时,运动时正常的心率增加被阻止,从而导致向运动肌肉的氧气输送受损;或在充血性右心衰竭时,运动时正常的每搏输出量增加受损;或在存在严重贫血时,血液的携氧能力受限,此时内脏血流量会大幅减少,血液会转向运动的肌肉组织。因此,只要所有其他代偿机制保持完整,在剧烈运动期间内脏血流通常会维持。然而,当任何其他代偿机制被破坏(即使是犬脾脏储备的消除)时,内脏血流就会减少并发生分流。

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