Nayler W G
Am J Pathol. 1981 Feb;102(2):262-70.
Ischemia of the myocardium results in a loss of ultrastructure and function. Tension generation is diminished or abolished, electrolyte imbalance occurs, and the ATP-generating capacity of the mitochondria is reduced. An intracellular accumulation of Ca2+ appears to precipitate many of these changes, the intracellular accumulation of Ca2+ being caused, in turn, by a failure of the ATP-dependent mechanisms responsible for maintaining intracellular homeostasis with respect to Ca2+. This hypothesis has been tested by the use of hypothermia, pretreatment with verapamil and a reduced extracellular Ca2+ to modify the events precipitated by an ischemic episode.
心肌缺血会导致超微结构和功能丧失。张力产生减弱或消失，出现电解质失衡，线粒体产生ATP的能力降低。细胞内Ca2+的积累似乎促成了许多这些变化，而细胞内Ca2+的积累又是由负责维持细胞内Ca2+稳态的ATP依赖机制失效所致。通过使用低温、维拉帕米预处理和降低细胞外Ca2+来改变缺血发作引发的事件，对这一假说进行了验证。
