Magnetic resonance (MR) may be used for repeatedly and non-invasively imaging the brain. Until now, no studies have used this approach to study the effects of carbon monoxide (CO) poisoning in a defined animal model. Conscious, Levine-prepared female rats (unilateral carotid artery and jugular vein occlusion) were exposed to 2400 ppm CO for 90 min, with or without the infusion of 50% glucose solution; CO-stimulated increases in blood glucose and lactate occurred in both groups, while blood pressure and body temperature fell. One to four hours following termination of CO exposure, increased cortical pixel intensity, cortical surface area and brain midline shift were observed on the operated side of the brain in some rats of both groups (i.e. responders = R), providing evidence of edema. At sacrifice, 5 h following termination of CO exposure, gross water content was increased on the left side in the corresponding cortical slices in R rats, providing another measure of edema. Significant positive correlations were found between left to right pixel intensity difference and water content difference, and between the extent of midline shift and water content difference. The elevations of blood glucose and lactate concentrations, and the magnitudes of CO-induced hypothermia and hypotension were similar to those in past studies, but appeared to exert no effect on the severity of cortical edema in terms of differences in pixel intensity, surface area, midline shift or gross tissue water content. Thus, the observed differences between the R rats and the non-R rats is not explained by the available data. The results of this study demonstrate that MR imaging can detect changes in the cerebral cortices of rats given an acute toxic challenge with CO. Moreover, in responders the edema develops quickly, reaching nearly full development within 1 h after CO exposure.
INTRODUCTIONCarbon monoxide (CO) is a poisonous gas that causes death, as well as a wide variety of immediate and delayed morbid effects, with nervous system damage being the most common. In the rat, acute CO poisoning is characterized by hypotension, bradycardia, hypothermia, hemoconcentration and hyperglycemia. 1-3 A recent study using the Levine-prepared rat demonstrated increased neurological deficit and general morbidity following 90 min of CO exposure in subjects experiencing elevated blood g l u c o~e .~ Similar findings were obtained from a retrospective study of human CO poisonings.s Thus, glucose level appears to be an important determinant of cerebral viability and overall survival during the hypoxia and the relative ischemia of CO poisoning. Whether elevated blood glucose permits an increased rate of glycolysis, generating more lactate and hence an increased blood and tissue acidosis, is unknown.Magnetic resonance (MR) is a recent, non-invasive technique for assessing brain structure, chemistry and the damaging effects of hypoxia, ischemia and toxic agents. Through the use of spectroscopic applications of nuclear MR, brain levels of high-energy phosphates t...
