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PAGE \* MERGEFORMAT 19
Adenosine preconditioning on myocardial protection of the delay
Study: LI Wen Ding Hui Wang Yang Jun Li Song Yong Li Li Jiang Yurong
[Abstract] The purpose of ATP sensitive potassium channel confirmed (KATP opening and endogenous nitric oxide synthase (iNOS upregulation mediated by adenosine (ADO) pretreatment delayed protection. Methods Experimental animals were randomly divided into 4 groups control group: 24 h before ischemia intravenously saline, ADOA1 receptor agonist (CCPA group: myocardial ischemia 24 h before the intravenous injection of drug CCPA pretreatment, glibenclamide (Gli group: myocardial ischemia 30 min intravenous Gli, CCPA / Gli group: CCPA group on the basis of treatment of myocardial ischemia and 30 min before intravenous injection of Gli. using isolated working heart model in rabbits, each group of myocardial ischemia were 30 min, 30 reperfusion min. observation of ischemia / reperfusion hemodynamics and cardiac function before and after the change. Determination of coronary effluent after reperfusion lactate dehydrogenase (LDH, creatine kinase (CPK, nitric oxide (NO) and myocardial adenosine triphosphate (ATP content. with triphenyl tetrazolium chloride (TTC) to determine the scope of myocardial infarction. reverse transcriptase polymerization chain determination iNOSmRNA. Results CCPA pretreatment significantly improve myocardial ischemia / reperfusion the recovery of cardiac function, and this protection Gli function is blocked, CCPA preconditioning reduces myocardial ischemia / reperfusion in coronary effluent LDH, CPK levels, and inhibit this protective effect of Gli, CCPA preconditioning can reduce myocardial infarct size, and is Gli blocked CCPA pretreatment increased the concentration of myocardial ATP, Gli could antagonize this effect, CCPA pretreatment slightly increased NO concentration in cardiac tissue, this effect is not Gli impact, CCPA pretreatment increased myocardial iNOS expression, t
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