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  • 期刊

Arrhythmogenic and Inotropic Effects of Lactic Acid in Canine Ventricular Tissues

乳酸對狗心室組織的節律不整及收縮力抑制作用

摘要


離體狗Purkinj纖維電生理研究的結果顯示,10mM乳酸抑制動作電位零期去極化速率,並減小收縮力。動作電位期間逐漸延長,電位負值減小,終於引起後電位(delayed afrerdepolarizations)及緩慢反應(slow responses)。以苛性鈉矯正酸鹼度後,乳酸塩不減小靜止膜電位負值,也不再引起後電位及緩慢反應,但仍然延長動作電位期閒(APD50)。在高鉀(16mM)溶液中,乳酸塩增加動作電位高度及期間,此作用在以氮氣取代氧氣之後仍然存在。乳酸塩雖可增加心室肌收縮張力,但抑制張力變化速率(dF/dt),收縮舒張期間則明顯延長,可見心肌收縮張力的增加是由於舒張過程較慢,而非收縮力(contractility)增加的後果。以上結果顯示,乳酸對Purkinj纖維的節律不整作用與氫離子抑制細胞膜鉀離子通透性(gk)有關。乳酸塩氧化所產生能量可幫助維持靜止膜電位,但似不能增加透過細胞膜的鈣離子內流,也不能增加心室肌收縮力。

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並列摘要


Lin, C. I., K. Y. Lin and H. H. Lu: Arrhythmogenic and inotropic effects of lactic acid in canine ventricular tissues. Chinese J. Physiol. 26(2):61-70, 1983. Effects of 10 mM lactic acid on the action potential of driven and spontaneously beating dog Purkinje fibers were studied in different [K](subscript o) Tyrode solution. The results show that lactic acid inhibits repolarization and induces afterdepolarizations and slow responses. These effects are accompanied by a depression of contractile force. After correction of pH, lactate still increases duration of the plateau of action potential but does not decrease maximum diastolic potential nor induce afterdepolarization. In high [K](subscript 0), lactate increases the upstroke and the duration of slow responses induced by electrical stimuli. These changes in slow responses could not be abolished by anoxia. In ventricular muscle fibers, lactate prolongs twitch duration but does not increase the dF/dt. The above findings suggest that a reduction of pH by lactic acid inhibits repolarization and induces slow responses through an inhibition of transmembrane K conductance. Lactate ion itself also appears to delay the activation of outward current i(subscript x). Oxidation of lactate may supply energy to maintain normal resting potential but does not appear to increase slow inward current in dog ventricular tissues.

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