Poole-Wilson P A
Ciba Found Symp. 1982;87:58-76. doi: 10.1002/9780470720691.ch4.
The contractility of heart muscle is sensitive to small and physiological changes of extracellular pH. The reduction of contractility associated with an acidosis is determined by the fall of pH in the intracellular fluid. The function of many organelles within the cardiac cell is affected by hydrogen ions. The tension generated by isolated myofibrils at a fixed calcium concentration is reduced at low pH. The dominant mechanism for the reduction of contractility in whole tissue is competitive inhibition of the slow calcium current by hydrogen ions. The reduction of the slow calcium current is similar when the same fall of developed tension is induced by acidosis or by a reduction of extracellular calcium concentration. Measurement of tissue pH with fast-responding extracellular electrodes show that, in myocardial ischaemia, tissue acidosis develops at the same time or only seconds before the onset of contractile failure. Much of the reduced contractility can be accounted for by the severity of the acidosis. Although a mild acidosis can delay or prevent damage to the myocardium from ischaemia or hypoxia, a severe acidosis is not beneficial and may even cause tissue necrosis.
心肌收缩力对细胞外pH值的微小生理变化敏感。与酸中毒相关的收缩力降低取决于细胞内液pH值的下降。心肌细胞内许多细胞器的功能受氢离子影响。在固定钙浓度下，低pH值时分离的肌原纤维产生的张力降低。全组织收缩力降低的主要机制是氢离子对慢钙电流的竞争性抑制。当酸中毒或细胞外钙浓度降低引起相同程度的张力下降时，慢钙电流的降低相似。用快速响应的细胞外电极测量组织pH值表明，在心肌缺血时，组织酸中毒与收缩功能衰竭同时发生或仅在其发作前几秒出现。大部分收缩力降低可由酸中毒的严重程度来解释。虽然轻度酸中毒可延迟或预防心肌缺血或缺氧造成的损伤，但严重酸中毒并无益处，甚至可能导致组织坏死。
