山莨菪碱对心肌缺血-再灌注损伤的保护作用和实验研究

Protective effects of anisodamine on myocardial ischemiareperfusion damage

用家犬制造实验性心肌缺血-再灌注动物模型,在心电图监测下,用间接和直接检测技术,在不同时间内分别检测汇常区,缺血-再灌注心肌的丙二醛(MDA)含量、谷胱甘肽过氧化物酶(GSH-px)及超氧化物歧化酶(SOD)的活性。结果,缺血-再灌注区心肌MDA高于正常区(P<0.05),GSH-px活性较正常区低,SOD活性在再灌注5min后持续上升,缺血30min后再灌注心肌标本直接低温测定电子自旋共振波谱显示氧自由基信号增强,提示心肌缺血后再灌注有氧自由基的异常增加,为心肌缺血一再灌注损伤的发生提供了依据。治疗组在再灌注前给子足量山莨菪碱,再灌后体内脂质过氧化损伤显著减轻,并呈量效关系。作者在临床抢救危重病患者28例取得满意效果,说明山莨菪碱能减少氧自由基的产生,防止膜的脂质过氧化损伤,提高细胞对缺血缺氧的耐受性。认为在再灌注的即时给予足量山莨菪碱配合其它抢救措施,可以预防或减轻再灌注损伤。

Oxygen free radicals are known be gentrated dur-ing the period of myocardial ischemia followed byreperrusion.It has been postulated that lipidperoxidation of membrane may play an important rolein ischemia reperfusion injury.In this study.the pro-tective effects of anisodamine on myocardial ischemicreperfusion injury has been investigated in experimen-tal dogs.The results of our experiments showed thatafter reperfusion,malondialdehyde(MDA)accumula-tion,decrease of GSH-px,histologic alteration andODFR signal detected by ESR were observed in thehearts of the dogs with ischemic-reperfusion injury.After reperfusion,significant MDA accumulated alsoit was.found that the free radicals caused the structuraldamage to myocytes in heart preparation.Treatmentwith anisodamine exhibited significant effect on thebiophysical,biochemical and histologic alteration inthe myocardia of the dogs.Clinically arrhythias werecorrected and abnormal electrocardiograms improved.Therapeutic effects of anisodamine has also been in-vestigated in our patients.Our results suggest thatanisodamines may be a ODFR scavenger for thetreatment of ischemia-reperfusion injury.