单甲氧基聚乙二醇—超氧化物歧化酶减轻低氧对兔心肌超微结构损伤

用雄性日本大耳兔（２．５￣３ｋｇ）每组５￣１２只，除常氧对照组外，其余各组分别模拟海拔高度５０００ｍ低压性低氧２４ｈ，左右心室肌超微结构损伤明显，主要表现为线粒体膜破损，嵴部分消的。肌丝间隙增大，肌原纤维断裂。溶酶体增多，糖原颗粒减少，氏氧前由股静脉注入单甲氧基聚乙二醇－超氧化物歧化酶的兔，肌原纤维排列整齐。线粒体含量丰富嵴密集，与肌原纤维基本呈平行。另测定低氧不同时间左右心室肌超氧化物歧化酶活性

MPEG-SOD ALLEVIATED THE DAMAGE OF HYPOXIA ON THE ULTRASTRUCTURE IN RABBIT'S MYOCARDIUM

There were 5-12 male rabbits (Japan big-ear species) in each group. All the groups except the normoxia groups were exposed to hypobaric hypoxia at an imitated altitude of 5000 m. During hypoxia for 24 h, the ultrastructure of both left and right myocardium was obviously damaged. Some mitochondria membranes were bursted, cristae mitochondriales deleted, and sarcomeres fractured and disintegrated. Lysosomes were increased and glycogen grains deereased. In MPEG-SOD group (monomethoxy polythylene glycol-superoxide dismutase. i. v. before hypoxia), myofibrils were in good order. Mitochondria were abundant and cristae mitochondriales concentrated. The arrangment of mitochondria was parallel to that of the myofibrils. The SOD (superoxide dismatase; EC 1. 15. 1. 1) activity and MDA (malondialdehyde) content were deter-minated during hypoxia for 24 h, 48 h and 72 h respectively. Only the increase of MDA of hypox-ia 24 h in the left myocardium showed statistical difference(P<0. 05, compared with normoxia). The results indicated that the decrease of SOD activity of both left and right myocardium was not obvious in the course of hypoxia. The results also suggested that superoxide radical (O2) played an important role in the damage of myocardium ultrastructure during hypoxia. The protection of of MPEG-SOD for myocardium may be due to the fact that MPEG-SOD inhibite lipid peroxide in the blood through scaveging the generated O2 in the blood during hypoxia.