Maruyama N
Department of Anesthesiology, National Takasaki Hospital.
Masui. 1996 Jan;45(1):59-65.
A histochemical study on the distribution of intrahepatic Cu-Zn SOD, Mn SOD and catalase was made using rat models for hemorrhagic shock. Hemorrhagic shock with an average blood pressure of 40 mmHg was created and blood was circulated again two hours later. Before the shock, Cu-Zn SOD was homogeneously distributed in hepatic lobuli; and, in cells, it was predominantly distributed in cytoplasms. With the progress of the shock, the number of Cu-Zn SOD began to decrease in the region around the central veins of liver; and, in cells, it came to be distributed predominantly in cell nuclei. Even after the circulation of blood, similar changes were observed. The changes of the distribution of Mn SOD were similar to those of Cu-Zn SOD. As to catalase before the shock, it was homogeneously distributed in lobuli; and, in cells, it was distributed in cytoplasms in the form of a minute granule. Unlike the cases of SODs, no significant change of the distribution of catalase was observed even after the progress of the shock. These results suggest that the functional decline in the protective system against active oxygen also relates to the cause of the progress of the cell injury even after the circulation of blood.
利用失血性休克大鼠模型,对肝内铜锌超氧化物歧化酶(Cu-Zn SOD)、锰超氧化物歧化酶(Mn SOD)和过氧化氢酶的分布进行了组织化学研究。制造平均血压为40 mmHg的失血性休克模型,两小时后再进行血液再灌注。休克前,Cu-Zn SOD在肝小叶中均匀分布;在细胞中,它主要分布在细胞质中。随着休克的进展,肝中央静脉周围区域的Cu-Zn SOD数量开始减少;在细胞中,它开始主要分布在细胞核中。即使在血液再灌注后,也观察到类似的变化。Mn SOD的分布变化与Cu-Zn SOD相似。至于休克前的过氧化氢酶,它在小叶中均匀分布;在细胞中,它以微小颗粒的形式分布在细胞质中。与超氧化物歧化酶的情况不同,即使在休克进展后,过氧化氢酶的分布也没有观察到明显变化。这些结果表明,即使在血液再灌注后,抗活性氧保护系统的功能下降也与细胞损伤进展的原因有关。