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作 者:胡长平[1] 李年生[1] 肖亮[1] 彭军[1] 邓汉武[1] 李元建[1]
出 处:《中南药学》2003年第2期67-70,共4页Central South Pharmacy
基 金:国家自然科学基金(No.30200361)
摘 要:目的 观察吴茱萸次碱对大鼠心肌缺血再灌注损伤的保护作用是否与激活辣椒素敏感的感觉神经有关。方法 大鼠在实验前10 min静脉注射吴茱萸次碱,然后结扎冠状动脉左前降支60 min,再灌注3 h。测定心肌梗死面积、血清肌酸激酶(CK)活性和血浆降钙素基因相关肽(CGRP)浓度。结果 吴茱萸次碱(100、300μg·kg-1,iv)能显著缩小心肌梗死面积,降低血清CK水平,升高血浆CGRP浓度。这些作用被预先给予竞争性辣椒素受体拮抗药Capsazepine(38 mg·kg-1,s.c.)或选择性感觉神经耗竭剂辣椒素(50 mg·kg-1,s.c.)所完全取消。结论 吴茱萸次碱对大鼠心肌缺血再灌注损伤有保护作用,其保护作用与通过激动辣椒素受体而激活辣椒素敏感的感觉神经有关。OBJECTIVE To determine whether the protection of rutaecarpine against myocardial ischemia-reperfu-sion injury is related to the activation of capsaicin-sensitive sensory nerves in rats. METHODS Rats were pretreated with rutaecarpine 10 min before the experiment, and then the left main coronary artery of rat hearts was subjected to 60-min occlusion followed by 3h reperfusion. The infarct area,activity of creatine kinase,and CGRP concentration in plasma were measured. RESULTS Pretreatment with rutaecarpine (100 or 300 μg · kg-1 ,i. v. ) significantly reduced the infarct area and creatine kinase release as well as a significant increase in plasma concentrations of CGRP. These effects of rutaecarpine were completely abolished by capsazepine (38 mg · kg -1 ,s. a ) ,a competitive vanilloid receptor antagonist,or by the pretreat-ment with capsaicin (50 mg · kg-1 , s. c. ),which selectively depleted transmitters in capsaicin-sensitive sensory nerves. CONCLUSIONS Rutaecarpine may protect against myocardial ischemia-reperfusion injury in rats and the protective effects of rutaecarpine are related to the activation of capsaicin- sensitive sensory nerves via activating vanilloid receptors.
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