NORMOBARIC AND HYPERBARIC-OXYGEN TREATMENT OF ACUTE CARBON-MONOXIDE POISONING IN RATS

Based on a model of acute carbon monoxide (GO) poisoning in rats with an occluded left carotid artery, we have evaluated the effects of norm obaric oxygen (NBO2) and hyperbaric oxygen (HBO2) on mortality and mor bidity. After exposure to 2,700 ppm CO in air for 1 h, the rats were g rouped and treated with air(group 1, untreated controls, in a previous study), 100 kPa O-2 for 4 h (group 2), 300 kPa normoxia (group 3, pre ssure controls), and 300 kPa O-2 (group 4) for 1 h, respectively. NBO2 started immediately, whereas HBO2 began 35 min after the end of the C O exposure. At the termination of the exposure, the four groups suffer ed identical levels of poisoning as indicated by the degrees of hypoth ermia, hypocapnia, drop in mean arterial pressure, and acidosis. Up to 48 h after the end of the CO exposure, mortalities were 76, 58, 75, a nd 17 in groups 1-4, respectively. The neurologic morbidities, indicat ed by abnormal motor behaviors and edema in the left cerebral hemisphe res, were 84, 67, 83, and 42% in groups 1-4, respectively. Compared to the normoxic treatments, the HBO2, but not the NBO2, significantly re duced the mortality and the neurologic morbidity. HBO2 was also signif icantly better than NBO2 in increasing surviving time and survival rat e. The results support the value of HBO2 in improving short-term outco me of acute CO poisoning in this rat model.