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机构地区:[1]武汉同济医科大学附属同济医院内科,武汉同济医科大学附属同济医院肝病研究所
出 处:《同济医科大学学报》1996年第5期346-349,共4页Acta Universitatis Medicinae Tongji
基 金:国家自然科学基金
摘 要:用新西兰大白兔制作急性肾缺血及再灌流损伤模型,观察肾组织细胞内三磷酸肌醇(IP3)、细胞内总钙及胞浆游离钙([Ca(2+)]i)浓度变化。结果显示,缺血组与对照组的IP3浓度(±s)分别为(430.3±46.8)、(297.9±54.3)min(-1),[ca(2+)]i浓度分别为(212.5±43.5)、(106.1±15.5)nmol/L,前者较后者均显著性升高(均为P<0.01),总钙浓度分别为(398.6±32.3)、(385.0±32.4)μmol/L,两组无显著性差异(P>0.05)。再灌流60min后IP3浓度为(776.0±68.0)min(-1)、[Ca(2+)]i浓度为(412.1±47.3)nmol/L、总钙浓度为(447.1±42.5)μmol/L,较对照组和缺血组均显著性增加(P<0.01)。提示,细胞内IP3对急性肾缺血及再灌流损伤中肾组织细胞内钙超负荷的形成具有重要作用。Acute renal ischemic damage and reperfusion injury models in rabbits were established. Concentratioh of IP3,total calcium, and [Ca(2+)]i in renal histocytes were observed.The results showed that concentrations of intracellular IP3 [(430.3±46.8),(297.9±54.3) min(-1),P<0.01] and [Ca(2+)]i [(212.5±43.5),(106.1±15.5) nmol/L,P<0.01] were increased in ischemic groups compared with the contrasted group,concentration of intracellular total calcium [(398.6±32.3),(385.0±32.4)μmol/L,P>0.05] was not increased obviously,whereas concentrations of intra cellular IP3 [(776.0±68.0) min(-1)]、[Ca(2+)]i [(412.1±47.3)μmol/L] and total calcium [(447.1±42.5)μmol/L, P<0.01]in reperfusion group (for 60 min) were increased remarkably as compared with the contrasted group and ischemic group.These data suggest that IP3 plays an important role in Ca(2+)-overloading forming of acute renal ischemic reperfusion injury.
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