title: [PROBLEM OF END EFFECTOR OF ISCHEMIC POSTCONDITIONING OF THE HEART].
abstract: It is well known that cardiovascular disease and in particular acute myocardial infarction are a major cause of death among working-age population in Russia. Some of the patients die after successful recanalization of the infarct-related coronary artery as a result of ischemic and reperfusion injury of the heart. It is obvious that there is an urgent need to develop new approaches to prevention reoxygenation heart damages. In this regard the study of adaptive phenomenon postconditioning is of particular interest. This analysis of literature source preformed by authors of the article indicates that main pretenders to the role of end-effectors of ischemic postconditioning of the heart are: (1) Ca(2+)-dependent K+ channel of BK-type (big conductance K+ channel), (2) mitoKATp channel (mitochondrial ATP-sensitive K+ channel), (3) MPT pore (mitochondrial permeability transition pore). At the same time, some investigators consider that mitoK(ATP) channel is only an intermediate link in the series of signaling events ensured an increase in cardiac tolerance to impact of ischemia-reperfusion. The most likely end effector of these three structures is MPT pore. Alternatively, it is possible, that unique molecular complex appearing a single end effector of postconditioning does not exist. Perhaps, that there are several effectors ensured cardioprotective effect of an adaptive phenomenon of postconditioning.
authors.forename: L N
authors.initials: LN
authors.lastname: Maslov
authors.forename: N V
authors.initials: NV
authors.lastname: Naryzhnaya
authors.forename: J-M
authors.initials: JM
authors.lastname: Pei
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
authors.forename: H
authors.initials: H
authors.lastname: Wang
authors.forename: I J
authors.initials: IJ
authors.lastname: Khaliulin
authors.forename: Yu B
authors.initials: YB
authors.lastname: Lishmanov
mesh_terms: D000818:Animals; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D057775:Ischemic Postconditioning; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D009206:Myocardium / Q000378:metabolism / Q000473:pathology