[Cardioprotective effects of atorvastatin preconditioning via iNOS upregulation in a rabbit ischemia/reperfusion model].
OBJECTIVE
To observe the preconditioning cardioprotection of atorvastatin (ATV) in rabbits underwent 40 min ischemia and 240 min reperfusion and to explore related mechanisms.


METHODS
The rabbits were randomized divided into Control group, ATV group (10 mg.kg(-1).d(-1) for 3 days before ischemia), ATV plus iNOS inhibitor S-methylisothiourea sulfate group (ATV + SMT group), SMT group, ATV plus mito K(ATP) channel blocker 5-hydroxydecanoate group (ATV + 5-HD group) and 5-HD group (n = 16 each group). The infarction size, CK-MB, LDH-1, nitric oxide synthase and mitochondrial ATP synthesization capacity ([ATP] m) were determined at the end of reperfusion.


RESULTS
Infarction size, CK-MB, LDH-1 were decreased by 26.3%, 31.4%, 19.1% and iNOS, [ATP] m increased by 102.6%, 46.8% post ATV compared to control group (all P < 0.05) and these effects could be blocked by cotreatment with SMT and 5-HD except the iNOS was not affected by 5-HD.


CONCLUSIONS
The atorvastatin preconditioning exerted cardioprotection by upregulating iNOS and activating mito K(ATP).
Zhou
Yi
Y
Department of Cardiology, Wuhan Central Hospital, Wuhan 430014, China.
Chen
Man-Hua
MH
Liu
Jin-Hua
JH
D000818:Animals; D000069059:Atorvastatin; D004195:Disease Models, Animal; D006538:Heptanoic Acids / Q000627:therapeutic use*; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism*; D015221:Potassium Channels; D011758:Pyrroles / Q000627:therapeutic use*; D011817:Rabbits; D015854:Up-Regulation
D006538:Heptanoic Acids; D015221:Potassium Channels; D011758:Pyrroles; D000069059:Atorvastatin; D052247:Nitric Oxide Synthase Type II