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急性败血症时脑脊液中喹啉酸、犬尿烯酸和L-犬尿氨酸增加。

Increased cerebrospinal fluid quinolinic acid, kynurenic acid, and L-kynurenine in acute septicemia.

作者信息

Heyes M P, Lackner A

机构信息

Section on Analytical Biochemistry, National Institute of Mental Health, Bethesda, MD 20892.

出版信息

J Neurochem. 1990 Jul;55(1):338-41. doi: 10.1111/j.1471-4159.1990.tb08857.x.

Abstract

Increases in brain quinolinic acid have been implicated in neurodegeneration and convulsions that may accompany infectious diseases. In three rhesus macaques (Macaca mulatta) with septicemia, both CSF and serum quinolinic acid concentrations were markedly elevated and were accompanied by increases in CSF kynurenic acid levels that were of a smaller magnitude. Elevated serum and CSF L-kynurenine concentrations also occurred and are consistent with activation of indoleamine-2,3-dioxygenase and increased substrate flux through the kynurenine pathway. Although it is probable that the marked increases in CSF quinolinic acid and kynurenic acid concentrations are reflected in the extracellular fluid space of brain, it remains to be determined whether the magnitude of such increases influences the activity of excitatory amino acid receptors in brain to produce excitotoxic pathology or noncytolytic disruption of functions mediated by excitatory amino acid receptors.

摘要

脑喹啉酸的增加与神经退行性变以及可能伴随传染病出现的惊厥有关。在三只患有败血症的恒河猴(猕猴)中,脑脊液和血清中的喹啉酸浓度均显著升高,同时脑脊液中犬尿酸水平也有较小幅度的升高。血清和脑脊液中L-犬尿氨酸浓度也升高,这与吲哚胺-2,3-双加氧酶的激活以及通过犬尿氨酸途径的底物通量增加一致。虽然脑脊液中喹啉酸和犬尿酸浓度的显著增加很可能反映在脑的细胞外液空间中,但这种增加的幅度是否会影响脑中兴奋性氨基酸受体的活性,从而产生兴奋性毒性病理或由兴奋性氨基酸受体介导的非细胞溶解性功能破坏,仍有待确定。

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