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Ultrastructural changes of the myocardial and striated muscle following a challenge of normobaric hyperoxia: the protective effects of alpha-tocopherol.

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.