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目的:运用激光扫描共聚焦显微镜观察不同浓度的布比卡因对KCl诱导的大鼠心室肌细胞内游离钙离子浓度([Ca2+]i)的影响,进而探讨布比卡因心肌抑制作用的可能机制。方法:培养新生SD大鼠心室肌细胞,将培养的心室肌细胞随机分为4组,分别为对照组(C组)、10μmol/L布比卡因组(B1组)、50μmol/L布比卡因组(B2组)、100μmol/L布比卡因组(B3组)。各组细胞均用钙荧光指示剂Fluo-3/AM染色,运用激光扫描共聚焦显微镜动态观察单个心室肌细胞内钙荧光强度(fluorescent intensity,FI)的变化。结果:与对照组比较10μmol/L的布比卡因对KCl诱导的大鼠心室肌细胞内钙FI变化无明显影响(P>0.05),50μmol/L和100μmol/L的布比卡因则明显抑制KCl诱导的钙离子跨膜内流(P<0.05);抑制程度B3组>B2组(P<0.05)。结论:低浓度的布比卡因对KCl诱导的大鼠心室肌细胞内[Ca2+]i的变化无明显影响,高浓度则明显抑制钙离子跨膜内流。布比卡因呈浓度依赖性抑制兴奋收缩耦联时心室肌细胞内游离钙离子内流,可能是其心肌抑制作用的原因之一。
OBJECTIVE: To observe the effects of different concentrations of bupivacaine on KCl-induced intracellular free calcium concentration ([Ca2 +] i) in rat ventricular myocytes by laser scanning confocal microscopy, and to explore the possible inhibitory effect of bupivacaine mechanism. Methods: The ventricular myocytes of neonatal SD rats were cultured and the cultured ventricular myocytes were randomly divided into 4 groups: control group (C group), 10 μmol / L bupivacaine group (B1 group), 50 μmol / L bupivacaine Ca2 + group (B2 group) and 100μmol / L bupivacaine group (B3 group). The cells in each group were stained with Fluorescence staining (Fluo-3 / AM), and the changes of intracellular calcium fluorescence (FI) in a single ventricular myocytes were observed by laser scanning confocal microscopy. Results: Compared with the control group, bupivacaine at 10μmol / L had no significant effect on KCl-induced intracellular calcium-induced changes in rat ventricular myocytes (P> 0.05), and the concentrations of 50μmol / L and 100μmol / L of bupivacaine were significantly Inhibition of KCl-induced transmembrane influx of calcium (P <0.05); inhibition of B3 group> B2 group (P <0.05). CONCLUSION: Low concentrations of bupivacaine have no significant effect on the changes of [Ca2 +] i in KCl-induced rat ventricular myocytes, while the high concentration of bupivacaine significantly inhibits the transmembrane infiltration of Ca2 +. Bupivacaine may be one of the reasons of its myocardial inhibition in a concentration-dependent manner to inhibit the influx of free calcium in ventricular myocytes during excitatory-contractive coupling.