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目的 观察不同浓度异丙酚和硫喷妥钠对氯化钾、异丙肾上腺素和咖啡因诱发的大鼠心肌细胞钙离子移动的影响 ,探讨其心肌抑制作用的机制。方法 用Fluo 3AM钙荧光指示剂染色培养的大鼠心肌细胞 ,在激光共聚焦显微镜下动态观察用药前和使用临床麻醉诱导峰浓度和 5倍诱导峰浓度的异丙酚 (5 0、2 5 0 μmol·L-1)和硫喷妥钠 (10 0、5 0 0μmol·L-1)后 ,氯化钾、异丙肾上腺素和咖啡因诱发的细胞内钙离子荧光强度的变化。结果 诱导峰浓度的异丙酚和硫喷妥钠减弱氯化钾和异丙肾上腺素诱发的钙离子跨膜内流 ,细胞内钙荧光强度的峰值下降 ,与对照组相比差异有显著性 (P <0 0 5 ) ,硫喷妥钠的抑制作用较异丙酚大。 5倍诱导峰浓度的异丙酚和硫喷妥钠使钙离子跨膜内流进一步降低。但两种浓度的异丙酚和硫喷妥钠对咖啡因诱发的细胞肌浆网内储存钙的释放、钙荧光强度的升高均无影响 (P >0 0 5 )。结论 异丙酚和硫喷妥钠呈浓度依赖地抑制电压门控和受体门控性钙通道的开放 ,钙离子跨膜内流 ,降低兴奋收缩耦联时细胞内钙离子浓度 ,这可能是其心肌抑制作用的原因之一 ,而对肌浆网的功能无明显影响
Objective To observe the effect of different concentrations of propofol and thiopental on the calcium ion transport in rat cardiomyocytes induced by potassium chloride, isoproterenol and caffeine, and to explore the mechanism of myocardial inhibition. Methods The cultured rat cardiomyocytes were stained with Fluo 3AM calcium fluorescence indicator, and observed under the confocal laser scanning microscopy under the confocal laser scanning microscope. Before propofol anesthesia, the concentration of propofol (5 0,2 5 0 The changes of intracellular calcium fluorescence induced by potassium chloride, isoproterenol and caffeine were observed after treatment with thiopental (100 micromol·L-1) and thiopental (10 0500 micromol·L-1). Results Propofol and thiopental, induced by peak concentration, attenuated the transmembrane influx of calcium ions induced by potassium chloride and isoproterenol, and decreased the peak of intracellular calcium fluorescence, which was significantly different from that of the control group P <0 0 5), thiopental inhibition than propofol. Propofol and thiopental at a 5-fold induction peak further reduced calcium transmembrane influx. However, propofol and thiopental at two concentrations had no effect on the release of calcium and the increase of calcium fluorescence in caffeine-induced sarcoplasmic reticulum (P> 0.05). Conclusions Propofol and thiopental inhibit the opening of voltage-gated and receptor-gated calcium channels in a concentration-dependent manner. The increase of calcium ion transmembrane influx and the decrease of intracellular Ca2 + concentration during excitatory and contractile coupling may be One of the reasons for its myocardial inhibition, but no significant effect on the function of sarcoplasmic reticulum