中文摘要：

目的研究M3受体激动剂毛果芸香碱对离体大鼠心肌缺血再灌注损伤的保护作用。方法采用Iangendoff灌注系统，建立离体大鼠心肌缺血再灌注损伤模型．、观察毛果芸香碱5μmol·L^-1对复灌后冠脉流量、心肌丙二醛（MDA）含量、心肌超氧化物歧化酶（SOD）活性和心肌梗死面积的影响。结果毛果芸香碱改善缺血再灌注后的冠脉流量，其中5min（P〈0．01）和10min（P〈0．05）的冠脉流量增加显著；降低心肌MDA含量（P〈0．05）并提高心肌SOD活性（P〈0．05）；缩小心肌梗死面积（P〈0.05）。上述作用可被选择性M3受体阻断剂4-diphenylacetoxy-N-methylpiperidine-methiodide（4-DAMP）3nmol·L^-1所逆转。结论M3受体激动剂毛果芸香碱通过激动心肌M3费体而对离体大鼠心肌缺血再灌注损伤起保护作用。

英文摘要：

OBJECTIVE To investigate the protective effects of M3 receptor agonist pilocarpine on myocardial ischemia-reperfusion injury in isolated rat hearts. METHODS The models of myocardial ischemia-reperfusion injury in isolated rat hearts were built by mounting the isolated rat hearts to Langendorff perfiJsion apparatus and making them ischemic for 25 min followed by being reper- fused for 30 min. The coronary flow, the content of myocardial malondialdehyde （MDA） , the activity of myocardial superoxide dismutase （SOD） and the myocardial infraet size were observed. RESULTS 5 μmol · L^-1 Pilocarpine increased the coronary flow ＇after being reperfused for5 rninand 10 min,which reached up to （5.7±1.2） mL·min^-1（P〈0.01）and （5.4±1.2） mL·min（P〈0.05）, respectively;by contrast,the coronary flow of the ischemia-reperfusion group reached up to （4. 1 ± 1.0） mL · min^-1 and （4. 1±0.8） mL · min^-1. Compared with the myocardial ischemial ischemia-reperfusion group,the content of myocardial MDA was decreased from （14. 3 ± 4. 1 ） μmol · g^-1 to （ 10. 1 ± 2. 5 ） μmol · g^-1 （ P 〈 0. 05 ） and the activity of myocardial SOD was increased from （ 128 ± 36 ） U · mg^-1 to （183 ± 65） U · mg^-1（ P 〈 0. 05 ） after an administration of pilocarpine. Meanwhile,the myocardial infract size was decreased from （37.8 ± 13.6 ） % to （ 24. 9 ± 6. 3 ） % （ P 〈 0. 05 ） after an administration of pilocarpine. However, the protective effects of pilocarpine on myocardial ischemia-reperfusion injury were inhibited by 3 nmol· L^-1 4-diphenylacetoxy-N-methylpiperidine-methiodide （4-DAMP） ,a selective M3 receptor antagonist. CONCLUSION M3 receptor agonist pilocarpine has a protective role in myocardial is-chemia-reperfusion injury of insolated rat hearts via stimulating myocardial M3 receptors.