Kozlov S N, Iasnetsov V S
Ukr Biokhim Zh (1978). 1978 Mar-Apr;50(2):218-21.
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.
在体外实验中,研究了大鼠脑组织中糖酵解过程的状态,这些脑组织因损伤诱发水肿,并给予尼古丁和单碘乙酸盐,以及预先注射酚妥拉明、苯那嗪、氯丙嗪和三氟拉嗪。结果显示,脑水肿是在糖酵解受到强烈抑制的背景下发展的,这与孵育介质中乳酸的初始含量无关。能预防水肿的酚妥拉明、苯那嗪和氯丙嗪有助于糖酵解过程维持在正常水平。对水肿无效的三氟拉嗪不能防止糖酵解受到抑制。相应酶系统活性降低导致的糖酵解抑制被认为是脑水肿发展的主要致病因素之一,因为它会导致细胞正常水电解代谢所需能量的缺乏。