摘要
目的 研究东莨菪碱的心肌保护作用 ,探讨其可能的机制。方法 将Wistar大鼠 2 4只随机分为对照组 (C组 ,n =12 ,用KHB进行灌注 )和实验组 (S组 ,n =12 ,用KHB+ 东莨菪碱进行灌注 ) ,建立离体缺血再灌注心脏模型 ,测定再灌注前后心功能、心肌组织中NO的含量、NOS同功酶 (iNOS、cNOS)的活性以及心肌NOS同功酶 (iN OS、cNOS)mRNA表达。结果 (1)S组心功能得到明显改善 ;(2 )形态学检查发现S组的心肌细胞结构保存明显优于C组 ;(3)S组再灌注后NO含量明显减少 ,iNOS活性显著下降 ,cNOS活性略有下降 ,iNOS的mRNA表达显著下降 ,而cNOS的mRNA改变不明显。结论 东莨菪碱对离体缺血再灌注大白鼠心脏具有较明显的保护作用。其机制可能为 :(1)通过阻断M受体 ,扩张血管、促进心肌收缩 ;(2 )保持心肌组织内的NO含量正常。
Objective To study cardiac protection of scopolamine in the isolated working rat heart after ischemia.reperfusion injury(IRI), and to clarify its mechanism.Methods Twenty four Wistar rats were randomly divided into two groups with 12 rats each.: control and scopolamine treated group. The isolated working rat heart models were established. Before and after reperfusion, data including cardiac function, NO in myocardium, myocardial cNOS and iNOS contents, the gene expressions of cNOS and iNOS mRNA, and the histological change of myocardium were also measured.Results 1)In scopolamine treated group, the cardiac function was improved. 2)After reperfusion, the value of NO and iNOS were obviously increased, cNOS value was slightly decreased, the gene expression of iNOS was markedly upregulated, and there was no change in gene level of cNOS in scopolamine treated group. 3) In scopolamine treated group, microstructure was better preserved.Conclusion In isolated working rat heart model, scopolamine can protect the myocardium from IRI. Its mechanism is proposed by: 1)scopolamine might have effect on vasodilatation and improve myocardial contraction by blocking receptor M; 2)keep NO in normal range.
出处
《同济大学学报(医学版)》
CAS
2002年第2期86-89,共4页
Journal of Tongji University(Medical Science)
基金
上海市浦东新区科委基金资助项目 (PK9917)
关键词
东莨菪碱
心肌缺血
再灌注损伤
scopolamine
myocardial ischemia
reperfusion injury