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目的探讨左-卡尼汀(L-CN)预处理对大鼠心肌缺血再灌注损伤(MIRI)的心肌保护作用及其可能的机制。方法36只Wistar大鼠随机分为3组,每组n=12。左-卡尼汀治疗组(L-CN):术前给予L-CN 200 mg·kg~(-1)·d~(-1)腹腔注射给药5天;缺血-再灌注组(IR):术前给予等量生理盐水腹腔注射5天;假手术组(P):术前处理同IR组。L-CN和IR两组大鼠在心电监护下结扎左前降支(LAD)30 min后松开结扎线,恢复心肌血流灌注3 h后处死动物,P组除LAD仅穿线不结扎外,所有操作同前两组。(1)三组均于术前和处死动物前从颈动脉抽血观察血浆肌酸激酶、MB同工酶(CK-MB)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。(2)实验结束处死大鼠前留取心肌标本,光镜下观察心肌病理学改变,TUNEL法测定心肌细胞的凋亡指数。结果(1)动物处死前,IR组MDA、CK-MB高于L-CN组(P＜0．01),而SOD低于L-CN组(P＜0．01)。(2)IR组心肌细胞凋亡指数明显高于L-CN组(P＜0．05)。(3)组织形态学观察(HE):IR组心肌纤维水肿、大部分断裂; L-CN组心肌纤维扭曲,但结构基本完整。结论L-CN预处理对大鼠MIRI具有一定的保护作用,其机制可能是通过抑制心肌脂质过氧化、减少心肌细胞凋亡。
Objective To investigate the myocardial protective effect of L-CN preconditioning on myocardial ischemia-reperfusion injury (MIRI) in rats and its possible mechanism. Methods Thirty - six Wistar rats were randomly divided into three groups with n = 12 each. Left-carnitine treatment group (L-CN): L-CN 200 mg · kg -1 · d -1 was given intraperitoneally for 5 days before operation; ischemia-reperfusion group ): The same amount of normal saline was given intraperitoneally before operation for 5 days. Sham operation group (P): preoperatively with IR group. L-CN and IR rats were ligated with left anterior descending (LAD) for 30 min after cardiac electrocardiographic monitoring. The ligature was released and the myocardium perfusion was resumed for 3 h before sacrifice. Animals in group P were only perfused with LAD without ligation, Operation with the first two groups. (1) The levels of creatine kinase, MB isoenzymes (CK-MB), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in all three groups before and during the preoperative and post- active. (2) Myocardial specimens were collected before sacrifice at the end of experiment, pathological changes of myocardium were observed under light microscope, apoptosis index of cardiomyocytes was measured by TUNEL method. Results (1) Before the animals were sacrificed, the MDA and CK-MB in IR group were higher than those in L-CN group (P <0.01), but lower in SOD group than those in L-CN group (P <0.01). (2) The apoptosis index of cardiomyocytes in IR group was significantly higher than that in L-CN group (P <0.05). (3) Morphological observation (HE): Myocardial fibroedema was mostly ruptured in IR group. Myocardial fibers were distorted in L-CN group, but the structure was basically intact. Conclusions L-CN pretreatment can protect MIRI in rats. The mechanism may be through inhibition of myocardial lipid peroxidation and decrease of cardiomyocyte apoptosis.