Effect of Hyperbaric Oxygen Therapy on the Neurotransmitter Changes in Carbon Monoxide Exposed Rat Striatum

J Korean Neurol Assoc > Volume 9(2); 1991 > Article

Journal of the Korean Neurological Association 1991;9(2): 141-156.

일산화탄소 폭로후 고압산소요법이 백서선조체의 신경전달물질 변화에 미치는 영향

한설희, 조수헌

충북대학교 신경과. 서울대학교 예방의학

Effect of Hyperbaric Oxygen Therapy on the Neurotransmitter Changes in Carbon Monoxide Exposed Rat Striatum

Seol Heui Han, M.D. Soo Hun Cho, M.D.*

Dep. Of Neurology, Chungbuk University Dep. Of Preventive Medicine, Seoul National University*

Abstract

The selective vulnerability of the basal ganglia to carbon monoxide(CO) is well recognized. And hyperbaric oxygen therapy(HBO) has long been accepted as a primary treatment for CO poisoning; however, the mechanism of action and objective methods to assess the therapeutic efhcacy of HBO have not been fully established. To evaluate the effect of HBO on the neurotransmitter changes in CO poisoning the striatal dopamine and its metabolites were measured in CO-intoxicated and HBO treated rats by high performance liquid chromatograpy with electrochemical detection. Male SpragueDawley rats, weighing 250-350 g were exposed to 4,500 ppm CO for 30 minutes and a group of them was treated with HBO(3 ATA, 30 miutes). The neostriatum of the rats were obtained and investigated according to the various time lapse after the cessation of CO exposure or the completion of HBO, The results are as follows: 1. The application of the routine HBO to the normal rat did not affect the levels of striatal neurotransmitters. 2. The concentration of striatal DA was markedly increased in CO-intoxicated rat during acute phase and it was reversed by HBO. But the effect did not last more than 24 hours. 3. In the delayed phase of experiment, the concentration of striatal DA tended to be decreased, which was partially thought to be due to the striatal injury, damage of striatonigral pathway or neuronal loss of substantia nigra by C0-intoxication.These results suggest that dopaminergic system might be implicated both in the pathogenesis of C0-induced striatal injury and the therapeutic efficacy of HB0.