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目的研究蝙蝠葛酚性碱(PAMD)对心肌缺血及缺血再灌注损伤的作用。方法用大鼠皮下注射异丙肾上腺素85 mg.kg-1造成心肌缺血模型,于造模前30 min灌胃给予生理盐水、PAMD(7.5,15或30 mg.kg-1)、地尔硫10 mg.kg-1或地奥心血康150 mg.kg-1,测定心肌缺血后乳酸脱氢酶(LDH)、肌酸激酶(CK)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量及病理学改变。离体大鼠心脏缺血30 min再灌注40 min,分别给予PAMD(1,10或100 mg.L-1)或地奥心血康100 mg.kg-1,测定心肌缺血再灌注后左室收缩压(LVSP)、左室舒张末压(LVEDP)和左室压最大变化速率(±dp/dtmax)、冠脉流量,测定心肌SOD活性和MDA含量。结果 PAMD显著降低缺血所致的LDH、CK和MDA升高,提高SOD活性,减轻心肌病理损伤。PAMD促进缺血再灌注末LVSP、LVEDP和±dp/dtmax等恢复,增加冠脉流量和SOD活性并降低MDA含量。结论 PAMD对心肌缺血及缺血再灌注损伤有保护作用,其机制可能与其抗氧化及改善心肌代谢有关。
Objective To study the effect of PAMD on myocardial ischemia and ischemia-reperfusion injury. Methods Rats were injected subcutaneously with isoproterenol 85 mg.kg-1 to induce myocardial ischemia. Rats were injected intragastrically with normal saline, PAMD (7.5, 15 or 30 mg.kg-1) (LDH), creatine kinase (CK), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured after myocardial ischemia with or without 10 mg · kg-1 of sulfur or 150 mg · kg- ) Content and pathological changes. The isolated rat hearts were subjected to ischemia 30 min and then to reperfusion 40 min. PAMD (1, 10 or 100 mg.L-1) or DiaoXueKangKang 100 mg.kg-1 were respectively administered to determine the left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and left ventricular pressure (± dp / dtmax), coronary flow, myocardial SOD activity and MDA content. Results PAMD significantly reduced ischemia-induced elevated levels of LDH, CK and MDA, increased SOD activity and decreased myocardial pathological damage. PAMD promoted the recovery of LVSP, LVEDP and ± dp / dtmax at the end of ischemia-reperfusion, increased coronary flow and SOD activity and decreased MDA content. Conclusions PAMD has a protective effect on myocardial ischemia and ischemia-reperfusion injury, and its mechanism may be related to its antioxidation and improvement of myocardial metabolism.