[Intensity of glycolysis with brain edema in rats and application of some pharmacological agents].
In the in vitro experiments the state of glycolytic processes was studied in the rat brain tissues with development of edema induced by injury and administered nicotine and monoiodoacetate as well as with preliminary introduction of phentolamine, benactyzine, aminazine and trifluoperazine. The brain edema is shown to develop against a background of sharp inhibition of glycolysis independent of the initial content of lactic acid in the incubation medium. Phentolamine, benactyzine and aminazine which prevent from the edema contribute to the normal level of the glycolytic processes. Trifluoperazine ineffective with edema does not prevent from glycolysis inhibition. Inhibition of glycolysis resulting from a decrease in the activity of the corresponding enzymic systems is supposed to be one of the main pathogenetic factors of the brain edema development as it leads to deficit of energy necessary for normal water-electrolytic metabolism in cells.
D000818:Animals; D001535:Benactyzine / Q000494:pharmacology; D001929:Brain Edema / Q000139:chemically induced / Q000378:metabolism*; D002746:Chlorpromazine / Q000494:pharmacology; D006019:Glycolysis / Q000187:drug effects*; D007461:Iodoacetates; D009538:Nicotine; D010646:Phentolamine / Q000494:pharmacology; D051381:Rats; D014268:Trifluoperazine / Q000494:pharmacology; D014882:Water-Electrolyte Balance
D007461:Iodoacetates; D014268:Trifluoperazine; D001535:Benactyzine; D009538:Nicotine; D002746:Chlorpromazine; D010646:Phentolamine
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