Thurston J H, Pollock P G, Warren S K, Jones E M
J Clin Invest. 1970 Nov;49(11):2139-45. doi: 10.1172/JCI106431.
After the intraperitoneal injection into young mice of 700-800 mg/kg of salicylate, brain glucose fell to one-third or less of control values despite normal plasma glucose levels; brain lactate was nearly doubled and there were small decreases in phosphocreatine (18%) and in glycogen (17%). ATP, pyruvate, alpha-ketoglutarate, and glutamate were unchanged. In liver, glycogen was reduced 79% and lactate was five times higher than in control animals; glucose, glucose-6-phosphate, and ATP were unchanged. Since salicylate uncouples oxidative phosphorylation, it is postulated that high energy phosphate in the brain is maintained near normal levels by a compensatory increase in cerebral glycolysis. Apparently the brain glucose level falls because the rate of utilization exceeds the rate at which glucose can be supplied from the blood. Concurrent administration of glucose with salicylate elevated brain glucose concentration and was associated with striking improvement in the condition and the increased survival of the animals. These findings stress the fact that in salicylate poisoning the supply of glucose to the brain may be inadequate even when blood glucose levels are normal.
给幼鼠腹腔注射700 - 800毫克/千克水杨酸盐后，尽管血浆葡萄糖水平正常，但脑葡萄糖降至对照值的三分之一或更低；脑乳酸几乎增加了一倍，磷酸肌酸（18%）和糖原（17%）略有下降。三磷酸腺苷（ATP）、丙酮酸、α-酮戊二酸和谷氨酸未发生变化。在肝脏中，糖原减少了79%，乳酸比对照动物高五倍；葡萄糖、6-磷酸葡萄糖和ATP未发生变化。由于水杨酸盐使氧化磷酸化解偶联，据推测，脑内高能磷酸通过脑糖酵解的代偿性增加而维持在接近正常的水平。显然，脑葡萄糖水平下降是因为利用速率超过了血液中葡萄糖的供应速率。同时给予葡萄糖和水杨酸盐可提高脑葡萄糖浓度，并与动物状况的显著改善和存活率增加相关。这些发现强调了这样一个事实，即在水杨酸盐中毒时，即使血糖水平正常，大脑的葡萄糖供应也可能不足。
