缺氧對心臟血管系統之影響

The Effects of Hypoxia on the Cardiovascular System

郭立(L. Kuo) ； 陳幸一(H. I. Chen)

《Journal of Medical Sciences》 4卷3期 (1982/01) Pp. 1347-1359

摘要

缺氧對心臟血管系統之影響非常複雜。本文首先闡述缺氧對心臟血管之直接影響，然後再討論神經系統之參與調節作用。在離體心臟，缺氧使竇房結之舒張期去極化斜率變小，並減慢自發性脈衝的產生速率。竇房結及房室結的動作電位幅度在缺氧時變小，但心房不受影響。這是因為急速缺氧抑制了心肌細胞之緩慢離子內流，但不影響快速鈉離子內流之結果。缺氧時也可造成竇房結及房室結之傳導速率變慢，房室結之有效不反應期顯著延長。心收縮力在缺氧時顯著減小，此乃缺氧時抑制了ATP合成的結果。缺氧引起肺循環系統血管收縮的原因可能是化學媒介物質所造成；這些化學媒介包括Catecholamines，Histamine及Angiotensin。缺氧引起體循環局部血管擴張之作用機轉有二：（1）氧氣之直接作用及（2）血管舒張物質之作用。冠狀動脈及腦部血管在缺氧時舒張反應最明顯，四肢的反應較小，而腎臟血管幾乎無血管舒張現象。局部血管舒張反應可使血流重新分布，重要器官藉此可以得到較多的血液供應。這種局部血管舒張現象在氧代謝需求量愈大的器官（如心臟及收縮狀態的薄股肌）反應愈明顯。缺氧時循環系統之神經調節已知有化學接受器反射，中樞性之升壓反應及自主神經之控制。化學接受器之反射作用造成骨骼肌及內臟器官收縮，但使冠狀動脈擴張。缺氧狀態，血壓主要是靠化學接受器之反射作用來維持。若此反射作用無法維持血壓，則缺氧再加上低血壓可造成中樞性之升壓反應，於是血壓不致下降過低。缺氧時自主神經在調節心臟血管系統方面扮演着重要的角色。缺氧時交感神經之興奮可增快心搏速率、心搏量、心輸出量及血壓，但減小周邊血管阻力。副交感神經之抑制在缺氧時扮演的角色是增加心搏速率及心輸出量。若交感與副交感神經完全被阻斷，則以上之缺氧反應完全消失。

並列摘要

Acute hypoxia exerts complex cardiovascular effects through interaction between the direct action and indirect reflex adjustments. In the isolated heart, hypoxia decreases the slope of diastolic depolarization in the SA node, and thereby reduces the spontaneous nodal rhythm. The amplitude of action potential in the SA and AV node is decreased during hypoxia, but the action potential in the atrium is little affected. The difference is attributed to the inhibitory effect of hypoxia on the slow inward current without significant effect on the fast sodium inward current. Hypoxia also depresses the nodal conduction, prolongs the effective refractory period of AV node, and reduces the ventricular contractility. The reduction in the contractile force is due to inhibition of ATP synthesis. In the pulmonary circulation, acute hypoxia elicits vasoconstriction presumably because of local release of chemical mediators. The potential chemical mediators include catecholamines, histamine and angiotensin. The mechanisms of hypoxia-induced vasodilatation in the systemic vascular beds operates through direct oxygen action and metabolic vasodilators action. Redistribution of blood flow is accomplished by a local effect of hypoxia which predominantly produces dilatation in coronary and cerebral vessels. The responses of limb vessels are small and renal vessels do not dilate even at very low PO2. It is apparent that the vasodilatory response to hypoxia has a preferential effect on organs that are highly active metabolically. Nervous control of circulation during hypoxia involves chemoreceptor reflex, central pressor effects and autonomic control. Chemoreceptor reflex induces vasoconstriction in the skeletal muscles and the splanchnic bed, while dilatation in coronary vessels. The arterial pressure is maintained primarily by the chemoreceptor reflex. If the chemoreceptor reflex fails to maintain arterial pressure, hypoxia and hypotension together will activate the central pressor response. The autonomic nervous system plays a major role in mediating cardiovascular response to hypoxia. The sympathoadrenergic activity increases heart rate, stroke volume, cardiac output and blood pressure, and may decrease total peripheral resistance by ß-adrenergic stimulation. On the other hand, parasympathetic inhibition during hypoxia gives rise to increased heart rate and cardiac output.