Local cerebral glucose utilization and cerebral blood flow following CO-intoxication in rats

To clarify the mechanisms of delayed neuronal dysfunction following carbon monoxide (CO)-intoxication, local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) were measured respectively in rats using [^<14>C]-autoradiographic methods. Behavioral changes were also observed for 14 days. CO-intoxication was induced with 0.1% CD for 2 hours under light halothane anesthesia. At the end of CO-inhalation CO hemoglobin was approximately 60%. There was no significant difference in the behavior judged by locomotor activity and emotional behavior for 14 days between the CO-intoxication and the shamoperated group. In the neocorticied, caudate n., pallidus, hippocampus (CAI) and hypothalamus, LCGU were significantly lower by 13 to 27% at 7 days and by 15 to 24% at 14 days than those in the sham-operated group, while they did not change significantly at 3 days. In the substantia nigra compacta, LCGU was transiently elevated by 14% at 7 days. LCBF measured at 14 days was significantly lower by 13 to 18% in the caudate n., pallidus and septal n. than those in the sham-operated group. These results demonstrated the delayed changes in LCGU as a reflection of neuronal dysfunction in the neocorticies, extrapyramidal and limbic systems following CO-intoxication.