Brain Monoamines in Cerebral Ischemic Edema, the Effect of Gamma-Hydroxy-Butyrate
The ischemically induced disturbances of monoamines metabolism may persist longer than those of energy metabolism3,4. Among the observed changes in the monoamines of the brain, the reduction of the 5-hydroxytryptamine (5-HT) levels correlated best with the formation of ischemic edema induced in gerbils by 15 minutes of bilateral common carotid artery occlusion and release9. This type of brain edema was ameliorated by treatment with γ-hydroxybutyrate (GHB) or its metabolite γ-butyrolactone (GBL)1. Both of these substances belong to the naturally occurring central nervous system depressants which affect various cerebral metabolic pathways including those of the neurotransmitters when given to normal animals14,18. In the gerbil model of ischemia, they were found not only to reduce the progression of edema but to spare the energy metabolism and increase the survival rate of the affected animals. Moreover, correlative studies showed that the GHB or GBL treatment was of greater benefit than hypothermia or pentobarbital1,13,15 Since the overall advantages of GHB or GBL could not be entirely explained on the basis of hypometabolism, which is the common denominator for each of these therapeutic agents19, we investigated the GHB effect on the cerebral monoamines in ischemic cerebral edema.
KeywordsTyrosine Hydroxylase High Pressure Liquid Chromatography Brain Edema Tryptophan Hydroxylase Bilateral Common Carotid Artery Occlusion
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