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目的研究M3受体激动剂胆碱(choline)对慢性心力衰竭(CHF)大鼠心肌的保护作用及可能的机制。方法CHF大鼠Ⅱ型胶原酶消化分离单个心肌细胞,全细胞膜片钳技术记录L-型钙电流(ICa-L)变化;激光扫描共聚焦技术观测细胞内钙([Ca2+]i)变化。结果膜片钳实验结果显示,与CHF组比较,choline组ICa-L电流密度明显增高(n=6,P<0.01);预敷U73122后加入choline,与choline组比较,ICa-L电流密度明显下降(n=6,P<0.01)。共聚焦实验结果显示,与CHF组比较,choline组[Ca2+]i明显升高(n=80,P<0.01);与choline组比较,U73122与choline共同孵育组[Ca2+]i升高幅度不明显(n=80,P<0.01)。预先给予4-DAMP可部分逆转choline升高ICa-L及[Ca2+]i的作用。结论M3受体对CHF大鼠的心肌保护作用可能是通过Gq/11-PLC途径开放L-型钙通道,促进Ca2+内流,使[Ca2+]i增加。
Objective To investigate the protective effect of M3 receptor agonist choline on myocardium of chronic heart failure (CHF) rats and its possible mechanism. Methods Single cardiomyocytes were isolated by collagenase digestion in CHF rats and the changes of L-type calcium current (ICa-L) were recorded by whole-cell patch clamp technique. The changes of intracellular calcium ([Ca2 +] i) were observed by laser scanning confocal microscopy. Results Compared with CHF group, the ICa-L current density was significantly increased in the choline group (n = 6, P <0.01). Choline was added after U73122 pre-treatment. Compared with the choline group, the ICa-L current density was significantly higher Decreased (n = 6, P <0.01). Confocal results showed that [Ca2 +] i in choline group was significantly higher than that in CHF group (n = 80, P <0.01). Compared with choline group, the increase of [Ca2 +] i in U73122 and choline group was not obvious (n = 80, P <0.01). Pre-administration of 4-DAMP partially reversed the effect of choline on ICa-L and [Ca2 +] i. Conclusion The myocardial protective effect of M3 receptor on CHF rats may be due to the opening of L-type calcium channels via Gq / 11-PLC pathway, promoting Ca2 + influx and increasing [Ca2 +] i.