论文部分内容阅读
目的:研究卡维地洛对血管紧张素Ⅱ(AngⅡ)诱导的人心房肌细胞内钙超载的拮抗作用。方法:急性分离单个人心房肌细胞。实验分4组:正常对照组; AngⅡ组:加入终浓度为0.1μmol/L的AngⅡ;卡维地洛组:加入终浓度为1μmol/L的卡维地洛; AngⅡ+卡维地洛组:卡维地洛1μmol/L与AngⅡ0.1μmol/L同时加入。以Fluo 3/AM荧光指示剂负载,应用激光共聚焦显微镜技术,分别于加入干预药物后即刻与15 min检测[Ca2+]i变化。结果:对照组和卡维地洛组人心房肌细胞内荧光强度和荧光光密度值较低。AngⅡ加入后即刻,细胞内荧光光密度值开始增加,15 min后细胞内荧光强度和荧光光密度值显著增高(P<0.05)。而AngⅡ+卡维地洛组细胞内荧光光密度值显著低于AngⅡ组(P<0.05)。结论:AngⅡ可引起人心房肌细胞内Ca2+超载,卡维地洛能显著减轻AngⅡ诱导的人心房肌细胞内Ca2+超载。
AIM: To investigate the antagonistic effect of carvedilol on calcium overload induced by angiotensin Ⅱ (Ang Ⅱ) in human atrial myocytes. Methods: Acute isolation of single human atrial myocytes. The experimental group was divided into four groups: normal control group, AngⅡgroup: adding AngⅡ at a final concentration of 0.1μmol / L; carvedilol group: carvedilol at a final concentration of 1μmol / L; AngⅡ + carvedilol group: Carvedilol 1μmol / L and Ang Ⅱ 0.1μmol / L at the same time added. The Fluo 3 / AM fluorescent indicator was loaded. The change of [Ca2 +] i was detected by laser scanning confocal microscopy immediately after adding the intervention drug and 15 min respectively. Results: The fluorescence intensity and fluorescence intensity of atrial myocytes in control group and carvedilol group were lower. Immediately after AngⅡ addition, the intracellular fluorescence density began to increase, and the intracellular fluorescence intensity and fluorescence optical density increased significantly after 15 min (P <0.05). The intracellular fluorescence intensity of AngⅡ + carvedilol group was significantly lower than that of AngⅡ group (P <0.05). Conclusion: Ang Ⅱ can cause overloaded Ca2 + in human atrial myocytes, and carvedilol can significantly reduce the Ca2 + overload induced by Ang Ⅱ in human atrial myocytes.