Normobaric and hyperbaric oxygen treatment of acute carbon monoxide poisoning in rats.

Abstract

Based on a model of acute carbon monoxide (CO) poisoning in rats with an occluded left carotid artery, we have evaluated the effects of normobaric oxygen (NBO2) and hyperbaric oxygen (HBO2) on mortality and morbidity. After exposure to 2,700 ppm CO in air for 1 h, the rats were grouped and treated with air (group 1, untreated controls, in a previous study), 100 kPa O2 for 4 h (group 2), 300 kPa normoxia (group 3, pressure controls), and 300 kPa O2 (group 4) for 1 h, respectively. NBO2 started immediately, whereas HBO2 began 35 min after the end of the CO exposure. At the termination of the exposure, the four groups suffered identical levels of poisoning as indicated by the degrees of hypothermia, hypocapnia, drop in mean arterial pressure, and acidosis. Up to 48 h after the end of the CO exposure, mortalities were 76, 58, 75, and 17 in groups 1-4, respectively. The neurologic morbidities, indicated by abnormal motor behaviors and edema in the left cerebral hemispheres, were 84, 67, 83, and 42% in groups 1-4, respectively. Compared to the normoxic treatments, the HBO2, but not the NBO2, significantly reduced the mortality and the neurologic morbidity. HBO2 was also significantly better than NBO2 in increasing surviving time and survival rate. The results support the value of HBO2 in improving short-term outcome of acute CO poisoning in this rat model.