急性心肌梗塞心肌非缺血区脂质过氧化增强

INVOLVEMENT OF ENHANCED LIPID PEROXIDATION ALSO IN NON-ISCHEMIC AREA OF THE RAT HEART WITH ACUTE MYOCARDIAL INFARCTION

本文测定了冠状动脉结扎造成急性心肌梗塞(MI)大鼠心肌缺血区、非缺血区以及肝脏脂质过氧化(LPO)产物-丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性以及血清MDA和皮质醇含量。MI后2h,不仅心肌缺血区,而且非缺血区及肝脏MDA含量均较对照组明显升高。且伴随SOD活性的降低。血清MDA和皮质醇含量也明显升高,且两者呈正相关关系。MI后24h及72h心肌缺血区MDA明显低于对照组,而非缺血区MDA仍较对照组高。本结果表明:LPO增强,在心肌缺血区仅发生于急性MI早期,而在非缺血区则贯穿于急性MI全程。

This paper reports that malondialdchyde (MDA),a lipid peroxidation (LPO) product, and superoxidedismutase (SOD) in ischemic, non--ischemicmyocardium and the liver as well as serum MDA andcortisol were measured in rats with and withoutmyocardial infartion (MI) by coronary ligation. At 2hours after MI, a higher content of MDA was showednot only in ischemic but also in non--ischemicmyocardium and the liver than that of the control being theaccompanied with the decrcase Of the activity of SOD.Serum MDA and cortisol content in MI rats also iner-cased over those of the control, In additon, the two indexes,serum MDA and cortisol, showed the positive correla-tiont At 24 and 72 hours after MI, MDA content wasnon--ischemic myocadium than that of the control.lower in ischemic myocardium, but still higher inThe results suggest that cnhanced LPO occurs only inthe very carly phase of acute MI in ischemic arca ofheart, but lasts in the whole period of acute MI innon--ischemic arca of the heart.