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目的 :研究心肌缺血再灌注损伤肌浆网、肌膜钙泵 (Ca2 + ATPase)功能变化。方法 :采用大鼠离体心脏模型应用电镜酶细胞化学及生化技术 ,研究缺血再灌注心肌肌浆网、细胞膜原位钙泵分布及活性变化。结果 :心肌细胞钙泵以高电子密度颗粒主要分布于肌浆网、肌膜等膜结构 ,缺血 30min钙泵反应产物显著减少 ,再灌注 30min及 6 0min酶进一步减少或缺失。生化钙泵活性测定显示心肌缺血 30min时为 (0 .0 48± 0 .0 10 ) μmol/mg·h-1,再灌注 6 0min为 (0 .0 6 9± 0 .0 18) μmol/mg·h-1,酶活性较对照组显著降低 (P <0 .0 1,P <0 .0 5 )。结论 :本研究揭示钙泵活性降低发生在心肌缺血期 ,钙泵功能抑制是心肌缺血再灌注损伤的重要环节 ,是亚细胞Ca2 + 紊乱的直接原因
Objective: To study the function of sarcoplasmic reticulum and calcium pump (Ca2 + ATPase) in myocardial ischemia reperfusion injury. Methods: Electron microscopic cytochemistry and biochemical techniques were used to study the distribution of sarcoplasmic reticulum and the in situ calcium pump in myocardial reperfusion injury in rats. Results: The calcium pump of cardiac myocytes was mainly distributed in the sarcoplasmic reticulum and sarcolemma with high electron density particles. The product of calcium pump reaction was significantly reduced at 30 min after ischemia, and the enzyme was further reduced or lost 30 min and 60 min after reperfusion. The results of biochemical calcium pump assay showed that the myocardial ischemia was (0. 48 ± 0. 0 10) μmol / mg · h-1 at 30min and 60min after reperfusion was (0. 069 ± 0. 0 18) μmol / mg · h-1, the enzyme activity was significantly lower than the control group (P <0.01, P <0.05). Conclusion: This study revealed that the decrease of calcium pump activity occurs during myocardial ischemia. The inhibition of calcium pump function is an important part of myocardial ischemia-reperfusion injury and is the direct cause of subcellular Ca2 + disorder