[Evolution of concept and metabolic basis of ischemic dysfunction of the myocardium].
Myocardial contractile function during acute as well as chronic ischemia is reduced due to activation of a number of metabolic energy protecting mechanisms. Their abolition during reperfusion, associated with oxidative stress and incomplete restoration of function may cause cellular apoptosis due to impairment of aerobic ATP resynthesis. Strategy of postischemic reperfusion of the heart should be based on the use of natural protective mechanisms providing preferential restoration of high energy phosphates. The state of mitochondria is decisive for survival or restoration of function of cells.
Kapel'ko
V I
VI
D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D017682:Myocardial Stunning / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D017382:Reactive Oxygen Species / Q000378:metabolism; D009626:Terminology as Topic
D017382:Reactive Oxygen Species