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目的:探讨风湿性心脏病(风心病)慢性心力衰竭时心肌细胞内肌浆网Ca2+转运功能变化的机制。方法:采用Westernblot法测定19例风心病患者(风心病组)和6例意外脑死亡者(对照组)心肌肌浆网钙泵蛋白和兰尼碱受体含量,同时采用草酸盐易化的肌浆网Ca2+摄取法测定两组心肌肌浆网的Ca2+摄取功能,采用测定“裸露”心肌束的咖啡因敏感性方法测定风心病患者心肌肌浆网的Ca2+释放功能。结果:风心病组钙泵蛋白和兰尼碱受体相对含量比对照组分别显著减少23%(P<0.01)和10%(P<0.05),心肌匀浆肌浆网Ca2+摄取量和摄取率也均显著低于对照组(P<0.05~P<0.01),并且风心病患者钙泵蛋白相对含量变化与肌浆网Ca2+摄取率变化呈显著正相关(r=0.81,P<0.01),“裸露”心肌束的相对Ca2+释放速率变化也明显低于正常水平,且与兰尼碱受体相对含量变化密切相关(r=0.67,P<0.05)。结论:风心病心肌细胞内肌浆网Ca2+摄取和释放功能下降的机制主要与肌浆网的Ca2+摄取和释放蛋白含量变化有关。
Objective: To investigate the mechanism of Ca2 + transport in sarcoplasmic reticulum (Ca2 +) in cardiomyocytes in patients with rheumatic heart disease (rheumatic heart disease) complicated with chronic heart failure. Methods: Western blotting was used to determine the content of cardiac muscle sarcoplasmic reticulum calcium receptor and the content of ryanodine receptor in 19 patients with rheumatic heart disease (rheumatic heart disease) and 6 patients with unexpected brain death (control group). Meanwhile, oxalate facilitated muscle Ca2 + uptake in cardiac sarcoplasmic reticulum was determined by Ca2 + uptake in plasma and Ca2 + release from cardiac sarcoplasmic reticulum in patients with rheumatic heart disease by caffeine sensitivity assay of “naked” myocardial bundle. Results: Compared with the control group, the relative content of calcium pumpkin and ryanodine receptor in patients with rheumatic heart disease were significantly decreased by 23% (P <0.01) and 10% (P <0.05), respectively. The Ca2 + (P <0.05 ~ P <0.01), and the relative content of calcium pump protein in patients with rheumatic heart disease and sarcoplasmic reticulum Ca2 + uptake rate was significantly positively correlated (r = 0.81, P <0.01). The changes of relative Ca2 + release rate in “naked” myocardial bundle were also significantly lower than normal, and were closely related to the relative content of ryanodine receptor (r = 0.67, P < 0.05). Conclusion: The mechanism of Ca2 + uptake and release in sarcoplasmic reticulum of rheumatic cardiomyocytes is mainly related to Ca2 + uptake and release of protein in sarcoplasmic reticulum.