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作 者:李素香[1] 金基焕[1] 杨宗伟[1] 李星云[1] 韩德万[2] 仪明光
机构地区:[1]延边医学院心血管研究室 [2]延边大学物理系 [3]中国原子能科学研究院
出 处:《延边医学院学报》1990年第4期245-248,共4页Journal of Medical Science Yanbian University
摘 要: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。(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.
分 类 号:R540.2[医药卫生—心血管疾病]
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