Vannucci Robert C, Brucklacher Robert M, Vannucci Susan J
Department of Pediatrics, The Pennsylvania State University College of Medicine, The Milton S. Hershey Medical Center, Hershey, PA, USA.
Dev Neurosci. 2005 Mar-Aug;27(2-4):185-90. doi: 10.1159/000085991.
To ascertain the regulation of glycolysis during perinatal hypoxia-ischemia, 7-day postnatal rats were subjected to unilateral common carotid artery ligation followed by hypoxia with 8% oxygen for up to 90 min. Brain concentrations of glucose, lactate, and key glycolytic intermediates were determined at specific intervals of hypoxia. During hypoxia-ischemia, anaerobic glycolysis increased to approximately 62% of its maximal capacity, which equates to a 135% stimulation of the glycolytic flux. The key regulatory enzymes, hexokinase, phosphofructokinase and pyruvate kinase, were all stimulated during hypoxia-ischemia, and there were no enzymatic rate limitations. The major rate-limiting step for glycolysis was the transport of glucose across the blood-brain barrier into the brain.
为了确定围产期缺氧缺血期间糖酵解的调节情况，对出生后7天的大鼠进行单侧颈总动脉结扎，然后在8%氧气的环境下缺氧长达90分钟。在缺氧的特定时间间隔测定大脑中葡萄糖、乳酸和关键糖酵解中间产物的浓度。在缺氧缺血期间，无氧糖酵解增加到其最大容量的约62%，这相当于糖酵解通量增加了135%。关键调节酶己糖激酶、磷酸果糖激酶和丙酮酸激酶在缺氧缺血期间均受到刺激，且不存在酶促速率限制。糖酵解的主要限速步骤是葡萄糖穿过血脑屏障进入大脑。
