Benzi G, Pastoris O, Dossena M
J Neurosci Res. 1982;7(2):193-201. doi: 10.1002/jnr.490070210.
Some metabolites (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate, citrate, alpha-ketoglutarate, succinate, fumarate, malate, glutamate, aspartate, gamma-aminobutyrate, glutamine, alanine, NH+4) were measured in rat cerebral cortex after 5 minutes of complete compression ischemia, as well as after 5, 15, or 30 minutes of recirculation following 5 minutes of ischemia. Complete ischemia induced a drop of glycolytic substrates and intermediates, consistent with the increase of lactate, succinate, alanine, and gamma-aminobutyrate, and with the decrease of malate, fumarate, and alpha-ketoglutarate. These events may be regarded as an expression of the activation of the gamma-aminobutyrate cycle and of the succinate cycle, where succinate itself, in the absence of O2, acts as a terminal electron acceptor. During post-ischemic recovery, cerebral parameters tended to normalize, except for the further increase of alanine and the still higher than normal content of both succinate and gamma-aminobutyrate, as an expression of the possible activation of the gamma-glutamyl and gamma-aminobutyrate cycles during recovery.
在完全性压迫性缺血5分钟后，以及在缺血5分钟后再灌注5、15或30分钟后，对大鼠大脑皮层中的一些代谢物（糖原、葡萄糖、6-磷酸葡萄糖、丙酮酸、乳酸、柠檬酸、α-酮戊二酸、琥珀酸、富马酸、苹果酸、谷氨酸、天冬氨酸、γ-氨基丁酸、谷氨酰胺、丙氨酸、NH₄⁺）进行了测量。完全性缺血导致糖酵解底物和中间产物减少，这与乳酸、琥珀酸、丙氨酸和γ-氨基丁酸的增加以及苹果酸、富马酸和α-酮戊二酸的减少相一致。这些事件可被视为γ-氨基丁酸循环和琥珀酸循环激活的表现，在无氧情况下，琥珀酸本身作为末端电子受体。在缺血后恢复过程中，除了丙氨酸进一步增加以及琥珀酸和γ-氨基丁酸含量仍高于正常外，大脑参数趋于正常，这表明恢复过程中γ-谷氨酰和γ-氨基丁酸循环可能被激活。
