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目的:探讨MCI-154的正变力机制.方法:用皂苷500或50 nag·L~(-1)破坏或保留肌浆网(SR)的蜕膜心肌标本.皂苷500 mg·L~(-1)蜕膜标本的张力-pCa关系曲线描述了心肌收缩蛋白Ca~(2+)敏感性,pCa_(50)是Ca~(2+)敏感性的指标;皂苷50 mg·L~(-1)蜕膜标本的咖啡因挛缩幅值是SR Ca~(2+)释放的指标.结果:1)在相同Ca~(2+)浓度下,MCI-154(0.1mmol·L~(-1))增强心肌Ca~(2+)激活张力,对收缩蛋白的Ca~(2+)敏感性具有明显的增敏效应,pCa_(50)由对照的5.54(5.30-5.79)升为5.84(5.54-6.14) (P<0.01,n=8);Hill系数n降低了0.29(P<0.01,n=8);2)在保留了SR的标本上,MCI-154不能引起SR内Ca~(2+)释放,并对咖啡因引起的挛缩幅值无显著影响(P>0.05).结论:MCI-154直接增强心肌收缩蛋白的Ca~(2+)敏感性,但对SR的Ca~(2+)释放无明显作用.
Objective: To investigate the positive transformation mechanism of MCI-154.Methods: Saponin 500 mg · L ~ (-1) was used to destroy or retain the decidual myocardium samples of sarcoplasmic reticulum (SR) 1) The tension-decay curve of decidual specimens describes the Ca 2+ sensitivity of myocardial contractile proteins, and pCa 50 is an indicator of Ca 2+ sensitivity. Saponin 50 mg · L -1 ), Decidual caffeine contracture amplitude is an indicator of SR Ca 2+ release.Results: 1) MCI-154 (0.1 mmol·L -1) ) Increased the activation of Ca ~ (2+) in myocardium, and had a significant sensitizing effect on Ca ~ (2+) sensitivity of contractile proteins. The value of pCa_ (50) was increased from 5.54 (5.30-5.79) to 5.84 (P <0.01, n = 8); Hill coefficient n decreased by 0.29 (P <0.01, n = 8); 2) MCI- (P> 0.05) .Conclusion: MCI-154 can directly increase the Ca2 + sensitivity of myocardial contractile proteins, but not Ca2 + No significant effect of release.