Ashraf M
Department of Pathology and Laboratory Medicine, University of Cincinnati Medical Center, OH 45267-0529.
Virchows Arch B Cell Pathol Incl Mol Pathol. 1987;54(1):27-37. doi: 10.1007/BF02899194.
The effects of oxygen-derived radical scavengers (ODRS) on the heart was investigated during the calcium paradox. Perfusion with Ca2+-free medium caused cell separation at the intercalated discs and changes in the endothelial cells. Upon Ca2+ reintroduction, a massive cell damage occurred. The cytosolic enzyme, creatine phosphokinase (CPK), was released in large amounts (p less than 0.001). The tissue adenosine triphosphate (ATP) was reduced to 3.7 mumol/g dry weight from the control value of 21.6 mumol/g dry weight and tissue Ca2+ content was increased threefold. The treatment with superoxide dismutase (SOD) and catalase (CAT) increased percentage of normal cells (62.2%) compared to nontreated Ca2+ paradox group (0.2%) and caused negligible leakage of CPK. Tissue ATP was preserved (p less than 0.03), and Ca2+ content was also reduced in the hearts treated with SOD and CAT (p less than 0.03). The cell membranes and vascular endothelium were well preserved in the hearts treated with SOD and CAT. Boiled SOD and CAT administered were totally ineffective. It is suggested that oxygen-active species may have a role in the Ca2+ paradox injury.
在钙反常期间研究了氧衍生自由基清除剂（ODRS）对心脏的影响。用无钙培养基灌注导致闰盘处细胞分离和内皮细胞变化。重新引入钙离子后，发生了大规模的细胞损伤。胞质酶肌酸磷酸激酶（CPK）大量释放（p＜0.001）。组织三磷酸腺苷（ATP）从对照值21.6μmol/g干重降至3.7μmol/g干重，组织钙含量增加了两倍。与未处理的钙反常组（0.2%）相比，用超氧化物歧化酶（SOD）和过氧化氢酶（CAT）处理增加了正常细胞的百分比（62.2%），并且导致CPK的泄漏可忽略不计。组织ATP得以保留（p＜0.03），在用SOD和CAT处理的心脏中钙含量也降低了（p＜0.03）。在用SOD和CAT处理的心脏中细胞膜和血管内皮保存良好。给予煮沸的SOD和CAT则完全无效。提示活性氧可能在钙反常损伤中起作用。
