Marie C, Bralet A M, Bralet J
Laboratoire de Pharmacodynamie et Physiologie Pharmaceutique, Faculté de Pharmacie, Université de Dijon, France.
J Cereb Blood Flow Metab. 1987 Dec;7(6):794-800. doi: 10.1038/jcbfm.1987.136.
1,3-Butanediol (BD) is converted in the body to beta-hydroxybutyrate, and previous studies have shown that hyperketonemia had beneficial effects in experimental models of generalized hypoxia. The aim of this study was to determine if BD would reduce brain damage following cerebral ischemia. A transient forebrain ischemia of 30-min duration was induced by the four-vessel occlusion technique in control and BD-treated rats (25 mmol/kg, i.p.; 30 min prior to ischemia). BD treatment led to significant improvement of neurologic deficit during the 72-h recovery period and reduced neuronal damage in the striatum and cortex but not in the CA1 sector of the hippocampus. Evaluation of cerebral energy metabolism before and at the end of the ischemic period showed that the treatment did not change the preischemic glycolytic and energy metabolite levels but attenuated the ischemia-induced metabolic alterations. It increased energy charge, phosphocreatine, and glucose levels, and reduced lactate accumulation. The decrease in brain lactate concentration might account for the beneficial effects of BD by minimizing the neuropathological consequences of lactic acidosis.
1,3 - 丁二醇（BD）在体内可转化为β - 羟基丁酸，先前的研究表明高酮血症在全身性缺氧实验模型中具有有益作用。本研究的目的是确定BD是否会减轻脑缺血后的脑损伤。采用四血管闭塞技术在对照组和BD处理组大鼠（腹腔注射25 mmol/kg；缺血前30分钟）中诱导持续30分钟的短暂性前脑缺血。BD处理导致在72小时恢复期间神经功能缺损显著改善，并减少了纹状体和皮质中的神经元损伤，但海马体CA1区未出现这种情况。对缺血期开始前和结束时的脑能量代谢进行评估表明，该处理并未改变缺血前的糖酵解和能量代谢物水平，但减轻了缺血诱导的代谢改变。它提高了能量电荷、磷酸肌酸和葡萄糖水平，并减少了乳酸积累。脑乳酸浓度的降低可能通过最小化乳酸酸中毒的神经病理学后果来解释BD的有益作用。
