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目的:研究IP复合32℃浅低温晶体停搏液保护状态对未成熟心肌缺血再灌注损伤细胞超微结构的影响。方法:应用Langendorff离体心脏模型,IP采用2次5min缺血、5min再灌注,实验分为IP+32℃浅低温组和单纯32℃浅低温组。心脏灌注St.ThomasⅡ停搏液,缺血30min,37℃再灌注30min。采用血流动力学、生物化学及立体定量方法分析IP的心肌保护效果及对心肌细胞超微结构的影响。结果:再灌注后30min,IP组的LVDP、+dp/dtmax、-dt/dtmax恢复率明显高于单纯32℃浅低温组(P<0.05)。再灌注末,IP组心肌ATP含量显著高于单纯32℃浅低温组(P<0.05)。IP组心肌MDA含量显著低于单纯32℃浅低温组(P<0.05)。IP组基本完好心肌细胞体积密度高于单纯32℃浅低温组(P<0.001),而严重损伤心肌细胞的体密度小于单纯32℃浅低温组(P<0.05),IP组心肌细胞间质体积密度小于单纯32℃浅低温组(P<0.05)。IP组心肌组织内皮细胞有显著变性的毛细血管断面计数显著高于单纯32℃浅低温组(P<0.05)。结论:IP复合32℃浅低温晶体停搏液对未成熟心肌缺血再灌注损伤细胞超微结构有较好的保护作用。
Objective: To study the protective effect of IP composite 32 ℃ mild hypothermia crystalloid cardioplegia on the ultrastructure of immature myocardial cells after ischemia-reperfusion injury. Methods: Langendorff isolated heart model was used. IP was administered twice for 5 min ischemia and reperfusion for 5 min. The experiment was divided into hypothermia group with IP + 32 ℃ and hypothermia group with 32 ℃. Cardiac perfusion St. Thomas II cardioplegia, ischemia 30min, 37 ℃ reperfusion 30min. The hemodynamic, biochemical and stereochemical methods were used to analyze the protective effect of IP on cardiomyocyte ultrastructure and myocardial ultrastructure. Results: The recovery rates of LVDP, + dp / dtmax and -dt / dtmax in IP group were significantly higher than those in hypothermia group at 32 ℃ (P <0.05) 30 min after reperfusion. At the end of reperfusion, ATP content in IP group was significantly higher than that in hypothermia group at 32 ℃ (P <0.05). The myocardial MDA content in IP group was significantly lower than that in simple hypothermia group at 32 ℃ (P <0.05). The volume density of cardiomyocytes in IP group was higher than that in hypothermia group at 32 ℃ (P <0.001), while the density of severely damaged cardiomyocytes was lower than that in hypothermia group at 32 ℃ (P <0.05) The density was lower than the simple low temperature group of 32 ℃ (P <0.05). In the IP group, the number of capillary cross-sections with significant degeneration of endothelial cells was significantly higher than that of the hypothermia group at 32 ℃ (P <0.05). Conclusion: IP composite 32 ℃ mild hypothermia crystalloid cardioplegia has a good protective effect on the ultrastructure of immature myocardial cells against ischemia-reperfusion injury.