Cascio W E, Johnson T A, Gettes L S
Department of Medicine, University of North Carolina at Chapel Hill, USA.
J Cardiovasc Electrophysiol. 1995 Nov;6(11):1039-62. doi: 10.1111/j.1540-8167.1995.tb00381.x.
Myocardial ischemia leads to significant changes in the intracellular and extracellular ionic milieu, high-energy phosphate compounds, and accumulation of metabolic by-products. Changes are measured in extracellular pH and K+, and intracellular pH, Ca2+, Na+, Mg2+, ATP, ADP, and inorganic phosphate. Alterations of membrane currents occur as a consequence of these ionic changes, adrenergic receptor stimulation, and accumulation of lactate, amphipathic compounds, and adenosine. Changes in the volume of the extracellular and intracellular spaces contribute further to the ultimate perturbations of active and passive membrane properties that underlie alterations in excitability, abnormal automaticity, refractoriness, and conduction. These characteristic changes of electrophysiologic properties culminate in loss of excitability and failure of impulse propagation and form the substrate for ventricular arrhythmias mediated through abnormal impulse formation and reentry. The ability to detail the changes in ions, metabolites, and high-energy phosphate compounds in both the extracellular and intracellular spaces and to correlate them directly with the simultaneously occurring electrophysiologic changes have greatly enhanced our understanding of the electrical events that characterize the ischemic process and hold promise for permitting studies aimed at developing interventions that may lessen the lethal consequences of ischemia.
心肌缺血会导致细胞内和细胞外离子环境、高能磷酸化合物以及代谢副产物积累发生显著变化。可检测细胞外pH值和钾离子、细胞内pH值、钙离子、钠离子、镁离子、三磷酸腺苷（ATP）、二磷酸腺苷（ADP）和无机磷酸盐的变化。这些离子变化、肾上腺素能受体刺激以及乳酸、两亲性化合物和腺苷的积累会导致膜电流改变。细胞外和细胞内空间容积的变化进一步导致主动和被动膜特性的最终扰动，这些扰动是兴奋性改变、异常自律性、不应期和传导改变的基础。电生理特性的这些特征性变化最终导致兴奋性丧失和冲动传导失败，并形成通过异常冲动形成和折返介导的室性心律失常的基础。详细描述细胞外和细胞内空间中离子、代谢物和高能磷酸化合物的变化，并将它们直接与同时发生的电生理变化相关联的能力，极大地增进了我们对表征缺血过程的电活动的理解，并有望开展旨在开发可能减轻缺血致命后果的干预措施的研究。
