[Neuroprotective and cardioprotective effects of hypothermic preconditioning].
The literature data testify the there is an early and delayed hypothermic preconditioning of brain. Neuroprotective effect of early hypothermic preconditioning is a result of activation of adenosine A1 receptors, KATP-channels. Ras protein and predetermined by a decrease in the synthesis of NO*. The infarct-sparing effect of delayed hypothermic preconditioning of brain is depended upon protein synthesis de novo. The presented data demonstrate that hypothermic preconditioning prevents cardiomyocyte necrosis in response to ischemia-reperfusion, improves pump function of the heart during reperfusion period, exerts an antiarrhythmic effect. The hypothermic preconditioning exerts more pronounced cardioprotective effect than ischemic preconditioning. The protective impact of hypothermic preconditioning is depended upon activation of protein kinase C, AMP-activated protein kinase (AMPK) and inhibition of MPT pore. The reactive oxygen species are triggers and mediators of hypothermic preconditioning of heart.
L N
LN
Maslov
I G
IG
Khaliulin
Iu K
IuK
Podoksenov
D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D007035:Hypothermia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D019157:Ischemic Preconditioning, Myocardial; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D009569:Nitric Oxide / Q000378:metabolism
D009569:Nitric Oxide