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本工作在离体大鼠等容收缩心脏模型上观察耗竭心脏细胞内糖原对心肌缺血再灌注损伤的影响。心脏富氧灌流30 min后,随机分为三组:Ⅰ、富氧组:富氧灌流75min。Ⅱ、对照组:常规K-H液富氧灌流15min,旷置30min,再灌流30min。Ⅲ、耗竭糖原组:先用充N_2(95%N_2:5%CO_2)的K-H液灌流15min,余同组Ⅱ。结果表明。耗竭心肌细胞内糖原可提高再灌注后心脏血液动力学的恢复;冠脉流出液中LDH活性及心肌组织MDA含量降低,线粒体及胞浆液中GSH-Px有较高的活性;心肌组织Na~+,Ca~(2+)超负荷减轻。说明耗竭心肌细胞内糖原可通过减少细胞内H~+的生成抑制Na~+/H~+交换,从而明显减轻心肌缺血再灌注损伤。
This work in isolated rat isovolumic contraction of the heart model to observe the depletion of cardiac glycogen on myocardial ischemia-reperfusion injury. Heart oxygen-rich perfusion after 30 min, were randomly divided into three groups: Ⅰ, oxygen-enriched group: oxygen-rich perfusion 75min. Ⅱ, control group: conventional K-H liquid oxygen-rich perfusion 15min, Kuang 30min, reperfusion 30min. Ⅲ, the depletion of glycogen group: first filled with N_2 (95% N_2: 5% CO_2) K-H liquid perfusion 15min, the same group Ⅱ. The results show. Depletion of cardiomyocyte glycogen can improve cardiac hemodynamic recovery after reperfusion; LDH activity in myocardial efflux and myocardial MDA content decreased, mitochondria and cytosolic GSH-Px have higher activity; myocardial tissue Na ~ +, Ca ~ (2 +) overload reduced. Destruction of glycogen in cardiomyocytes can inhibit Na ~ + / H ~ + exchange by reducing intracellular H ~ + production, thus significantly reduce myocardial ischemia reperfusion injury.