Hatzenikolaou K P, Giala M M, Paradelis A G, Chatzinikolaou P K
Department of Anesthesia, University Campus, Thessaloniki, Greece.
Methods Find Exp Clin Pharmacol. 1995 Oct;17(8):509-18.
Normobaric hyperoxia has known deleterious effects on survival, presumably due to the generation of superoxide anion and hydrogen peroxide. To investigate the anatomical substrate of the effect of normobaric hyperoxia on the myocardial and striated muscles and the protective effect, if any, of alpha-tocopherol (vitamin E) on these tissues, we administered 95-99% O2 to adult male Wistar rats for 24, 48, 60 and 72 h. The animals were divided into four groups: 1) control I: six rats which breathed room air were used as controls for the ultrastructural studies; 2) control II: 10 rats which breathed 95-99% of O2 for up to 72 h were used as controls for arterial pressure, blood gases/pH, PvO2 and Hb measurements; 3) group A: hyperoxia: 24 rats divided into four subgroups according to the time of exposure to hyperoxia, A24, A48, A60, A72; and 4) group B: alpha-tocopherol/hyperoxia: 24 rats treated with alpha-tocopherol, 15 mg/kg/day, for 14 days before the beginning and throughout the period of hyperoxia, were divided into four subgroups (B24, B48, B60, B72) according to the time of exposure to hyperoxia. Our results showed that: 1) up to the 60th hour, arterial pressure (MAP) was satisfactory; PaO2 > 280 mmHg; PaCO2, pH and Hb were within normal limits; 2) ultrastructural studies of the myocardial apex, the diaphragm and the quadriceps femoris showed dilatation of the sarcoplasmic reticulum/T-tubuli system, swelling of mitochondria, and structural derangement of myofibrils, in particular in the z-bands. The findings were proportionally related to the time of exposure of hyperoxia. They were also more intensely shown on myocardial and diaphragmatic fibers in group A; 3) the survival time (mean +/- SD) was 63.8 +/- 2.5 h in group A and 68.9 +/- 3.8 h in group B. These results suggest that normobaric hyperoxia exerts a cytotoxic effect on the myocardial and striated muscle fibers and that the administration of alpha-tocopherol may delay or change the development of oxygen toxicity.
常压高氧对生存率具有已知的有害影响，推测这是由于超氧阴离子和过氧化氢的生成所致。为了研究常压高氧对心肌和横纹肌影响的解剖学基础以及α-生育酚（维生素E）对这些组织的保护作用（如果有的话），我们对成年雄性Wistar大鼠给予95 - 99%的氧气，持续24、48、60和72小时。动物被分为四组：1）对照组I：六只呼吸空气的大鼠用作超微结构研究的对照；2）对照组II：十只呼吸95 - 99%氧气长达72小时的大鼠用作动脉压、血气/pH、静脉血氧分压（PvO2）和血红蛋白（Hb）测量的对照；3）A组：高氧组：24只大鼠根据高氧暴露时间分为四个亚组，即A24、A48、A60、A72；4）B组：α-生育酚/高氧组：24只大鼠在高氧开始前14天及整个高氧期间每天给予15 mg/kg的α-生育酚，根据高氧暴露时间分为四个亚组（B24、B48、B60、B72）。我们的结果表明：1）直到第60小时，动脉压（平均动脉压，MAP）正常；动脉血氧分压（PaO2）> 280 mmHg；动脉血二氧化碳分压（PaCO2）、pH和血红蛋白均在正常范围内；2）对心肌尖部、膈肌和股四头肌的超微结构研究显示肌浆网/T小管系统扩张、线粒体肿胀以及肌原纤维结构紊乱，尤其是在Z带。这些发现与高氧暴露时间成比例相关。在A组的心肌和膈肌纤维中表现得更为明显；3）A组的生存时间（平均值±标准差）为63.8±2.5小时，B组为68.9±3.8小时。这些结果表明常压高氧对心肌和横纹肌纤维具有细胞毒性作用，并且给予α-生育酚可能会延迟或改变氧中毒的发展。
