[Cardioprotective effects of atorvastatin preconditioning via iNOS upregulation in a rabbit ischemia/reperfusion model]

Zhonghua Xin Xue Guan Bing Za Zhi. 2007 Nov;35(11):1041-5.
[Article in Chinese]

Abstract

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.

Conclusion: The atorvastatin preconditioning exerted cardioprotection by upregulating iNOS and activating mito K(ATP).

MeSH terms

  • Animals
  • Atorvastatin
  • Disease Models, Animal
  • Heptanoic Acids / therapeutic use*
  • Ischemic Preconditioning, Myocardial / methods*
  • Male
  • Myocardial Reperfusion Injury / metabolism
  • Myocardial Reperfusion Injury / prevention & control*
  • Nitric Oxide Synthase Type II / metabolism*
  • Potassium Channels
  • Pyrroles / therapeutic use*
  • Rabbits
  • Up-Regulation

Substances

  • Heptanoic Acids
  • Potassium Channels
  • Pyrroles
  • Atorvastatin
  • Nitric Oxide Synthase Type II