【摘要】 目的:观察丹参酮ⅡA磺酸钠对家兔缺血预适应心肌的保护作用。方法:随机将家兔24只分为心肌缺血组(IR)、缺血预适应组(IPC)和丹参酮ⅡA磺酸钠联合缺血预适应组(DS-201+IPC)。应用心外膜单相动作电位(MAP)探针记录技术检测缺血-再灌注过程中心肌复极50%时程(MAPD50)及心律失常发生率和持续时间;TTC染色测定梗死面积;HE染色病理组织学观察。结果:与IR组相比,IPC组缺血5min时的MAPD50迅速缩短(P<0.05),缺血20min时的MAPD50缩短明显减小(P<0.05),复灌30min后MAPD50的过度延长程度明显减小(P<0.05)。同时,缺血-再灌注中室性心律失常发生率明显降低(P<0.05)。在DS-201+IPC组,缺血5min时未见MAPD50迅速缩短(P>0.05),缺血20min及复灌30min后MAPD50及缺血-再灌注中室性心律失常发生率与IPC组无差异(P>0.05)。病理学检测显示,IPC组心肌梗死面积及组织损伤程度均明显小于IR组。DS-201+IPC组心肌梗死面积及组织损伤程度均小于IPC组。结论:①DS-201联合IPC取消了缺血早期IPC显著缩短MAPD50的效应,但对IPC抗缺血-再灌注心律失常作用无显著影响;②DS-201能增强IPC缩小心肌梗死面积和减轻组织损伤的作用。更多还原

【Abstract】 Objective: To investigate the effect of sodium tanshinon ⅡA sulonate on cardiaoprotection of ischemia preconditioning in rabbits. Methods: Twenty-four rabbits were divided into three groups randomly: IR(ischemia-reperfution)group, IPC(ischemia-preconditioning)group, DS-201+IPC(treatment with DS-201 before IPC)group.With the recording techniques of monophasic action potential(MAP), the effects of sodium tanshinon ⅡA sulonate in conjunction with ischemia preconditioning on MAPD50 (50% of duration of MAP) and the incidence of arrhythmia were examined. Myocardial infarct size was determined by staining with triphenylterazolium chloride;Morphological structure was observed. Results: In IPC group, compared with IR group, at 5 min after ichemia the MAPD50 were significantly decreased(P<0.05), the decreased degree of MAPD50 at 20 min after ischemia was reduced(P<0.05), and the excessive width of MAPD50 in reperfusion was limited(P<0.05),at the same time,the incidence of ventricular arrhythmias was totally suppressed(P<0.05). In IPC+DS-201 group, the reduction of MAPD50 at 5min after ischemia was abolished(P>0.05), the MAPD50 and the incidence of arrhythmias induced by is chemia-reperfusion were similar to that in IPC group at 20 min after ischemia and reperfusionin(P>0.05). The degree of reduction in infarct size and morphological injury of myocardium were more significantly in IPC group than that in IR group. The degree of reduction in infarct size and morphological injury of myocardium were more significantly in IPC+DS201 group than that in IPC group. Conclusions: The results suggest (1)At 5min after ischemia, DS-201+IPC abolishes the reduction of MAPD50 in IPC group, but dose not influence the antiarrhymic effects of IPC. (2)DS-201+IPC significantly enhances the effects of IPC on reduction of infarct size(P<0.05)and the morphological injury of myocardium.更多还原