Effect of dexmedetomidine postconditioning on mitochondria injury during myocardial ischemiia-reperfusion in isolated rat hearts / 中华麻醉学杂志

ABSTRACT

ObjectiveTo investigate the effect of dexmedetomidine postconditioning on mitochondria injury during myocardial ischemia-reperfusion (I/R) in isolated rat hearts.Methods Healthy female Wistar rats weighing 220-250 g were anesthetized with intraperitoneal 3％ pentobarbital 50 mg/kg and heparin 500 U/kg.Their hearts were excised and perfused in a Langenorff apparatus with modified K-H solution saturated with 95％ O2-5％ C02 at 37 ℃.Forty isolated rat hearts were randomly divided into 5 groups( n =8 each) I/R group(group A),dexmedetomidine 10 nmol/L group ( group B),dexmedetomidine 100 nmol/L group ( group C ),atractyloside ( the mitochondrial permeability transitionpore (mPTP) opener) group (group D)and dexmedetomidine 100 nmol/L + atractyloside group(group E).Myocardial I/R injury was induced by 40 min of global ischemia followed by 60 min of reperfusion.10 nmol/L dexmedetonidine( group B),100 nmol/L dexmedetonidine (group C),20 μmol/L atractyloside(group D) or 100 nmol/L dexmedetomidine + 20 μmol/L atractyloside (group E) was added into K-H solution and perfused for 10 min at the beginning of reperfusion.The myocardial tissues were obtained and mitochondria were isolated at the end of reperfusion for determination of activity of SOD,Na+ -K+ -ATPase,and Ca2+ -ATPase and content of MDA and Ca2+.ResultsThe activity of SOD,Na+ -K+ -ATPase and Ca2+ -ATPase was significantly higher and MDA and Ca2+ content lower in groups B and C than in group A( P ＜ 0.05).The activity of SOD,Na+ -K+ -ATPase and Ca2+ -ATPase was lower and MDA and Ca2+ content higher in groups E and D than in group C (P ＜ 0.05).There was no significant difference in activity of SOD,Na+ -K+ -ATPase and Ca2+ -ATPase and MDA and Ca2+ content between groups B and C,and between groups A and D( P ＞ 0.05).Conclusion Dexmedetomidine postconditioning can reduced mitochondria injury during myocardial I/R in isolated rat hearts through inhibiting of mPTP opening.