Köppel H, Klein W, Grisold M, Gasser R
Department of Physiology and Pharmacology, University of Leicester, United Kingdom.
Acta Med Austriaca. 1997;24(3):114-21.
In early myocardial ischemia we find several characteristic electrical and ionic alterations, like action potential shortening K(+)-accumulation or contractile failure. Trautwein and Dudel were 1954 the first to discuss action potential shortening as an important characteristic of myocardial ischemia. They already demonstrated that the action potential shortening is due to an enhanced outward current, while recently KATP-channels have been found to play an important role in the context. It has been suggested that contractile failure due to myocardial ischemia is caused by the shortening of action potential duration, reduced cytoplasmic free calcium levels, intracellular acidification, and a rise in inorganic phosphate and Mg. All of these phenomena may be related to the opening of KATP-channels. The different ionic and molecular mechanisms of contractile failure in myocardial ischemia will be discussed in this paper.
在早期心肌缺血时，我们会发现一些特征性的电和离子改变，如动作电位缩短、钾离子蓄积或收缩功能衰竭。1954年，特劳特魏因和杜德尔首次讨论了动作电位缩短是心肌缺血的一个重要特征。他们已经证明动作电位缩短是由于外向电流增强所致，而最近发现ATP敏感性钾通道在这一过程中起重要作用。有人提出，心肌缺血导致的收缩功能衰竭是由动作电位时程缩短、细胞质游离钙水平降低、细胞内酸化以及无机磷酸盐和镁含量升高引起的。所有这些现象可能都与ATP敏感性钾通道的开放有关。本文将讨论心肌缺血时收缩功能衰竭的不同离子和分子机制。
