ATP-MgCl_2、超氧化物歧化酶和异搏定对离体缺血再灌注鼠心肌线粒体钙离子的影响

本文以液体闪烁谱仪计数法,测定离体缺血再灌注鼠心肌线粒体内~(45)Ca~(2+)的放射强度(cpm),观察ATP-MgCl_2、超氧化物歧化酶(SOD)和异搏定对缺血再灌注鼠心肌线粒体内钙离子的影响。结果表明,ATP-MgCl_2,SOD和异搏定组的~(45)Ca~(2+)cpm显著低于对照组的~(45)Ca~(2+)cpm(P<0.01),ATP-MgCl_2,组和SOD组的~(45)Ca~2+cpm又低于异搏定组的~(45)Ca~(2+)cpm,而ATP-MgCl_2组和SOD组之间无显著性差异(P>0.05),结果提示,ATP-MgCl_2、SOD和异搏定三种药物均能阻止离体大鼠心肌线柱体内Ca~(2+)积聚,从而保护心肌细胞缺血再灌注性损伤。

Effects of ATP-MgCl_2, SOD and verapamil om mitochondral (45)~Ca~(2+) in isolated myocardium of the rat with ischemia-reperfusion

(45)~Ca~(2+) radiation intensity (cpm)was measured using liquid scintillation counting method, and the effects of ATP-MgCl_2, superoxide dismutase(SOD)and verapamil om mitochondrial (45)~Ca~(2+) in isolated myocardium of the rat with experimental ischemia reperfusion were studied respectively. It demonstrates that the (45)~Ca~(2+) cpms in ATP-MgCl_2, SOD, and verapamil groups were significantly weaker than that in control groups, and the cpms in ATP-MgCl_2 and SOD groups were weaker than that in verapamil group. The results suggest that ATP-MgCl_2, SOD, and verapamil can inhibit the accumulation of mitochondrial (45)~Ca~(2+) in myocardium induced by ischemia-reperfusion; these effects of ATPMgCl_2 and SOD are superior to that of verapamil.