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

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

用雄性日本大耳兔(2.5～3 kg)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,嵴部分消失.肌丝间隙增大.肌原纤维断裂.溶酶体增多,糖原颗粒减少.低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和丙二醛含量,除低氧24 h左心室肌丙二醛增加有统计学意义外,其余丙二醛含量增加和超氧化物歧化酶酶活性下降均无统计学意义.提示,超氧自由基(O_2^-)在低氧导致兔心室肌超微结构损伤过程中起重要作用,可能主要在低氧初期,单甲氧基聚乙二醇-超氧化物歧化酶清除了血液中增殖的过量O_2^-,抑制血液中脂质过氧化反应,因而保护心肌超微结构免受低氧伤害.

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.