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本工作用大鼠离体灌流心脏血再灌注损伤模型观察了K_(ATP)通道开放剂克罗卡林(Cromakalim,CRK)的心脏保护作用。结果表明,CRK能明显减少缺血再灌注损伤心肌的LDH及蛋白的漏出(P<0.01),降低脂质过氧化产物MDA的含量(P<0.01),心肌组织及心肌线粒体钙含量也显著降低(P<0.01)。CRK明显抑制心肌线粒体的最大~(45)Ca~(2+)摄取量及摄钙速率。CRK的上述作用均能被K_(ATP)通道阻断剂格列苯脲(Glybenclamide,GLB)所消除。上述结果表明,CRK能通过开放K_(ATP)通道发挥心脏保护作用,其心脏保护作用的机制可能与膜稳定作用、抑制氧自由基的产生及抑制心肌细胞和心肌线粒体钙超载有关。
This study was designed to investigate the cardioprotective effects of a K (ATP) channel opener, Cromakalim (CRK), on a rat model of perfused cardiac reperfusion injury. The results showed that CRK could significantly reduce the LDH and protein leakage (P <0.01), decrease the content of lipid peroxidation product (P <0.01) and the content of myocardial mitochondrial calcium in myocardium (P <0.01). CRK significantly inhibited maximal ~ (45) Ca ~ (2 +) uptake and calcium uptake in myocardial mitochondria. All of the above effects of CRK can be eliminated by Glybenclamide (GLB), a K (ATP) channel blocker. The above results indicated that CRK can exert cardioprotection through opening K (ATP) channel and the mechanism of its cardioprotection may be related to membrane stabilizing effect, inhibiting the production of oxygen free radicals and inhibiting calcium overload in myocardial cells and myocardial mitochondria.