Penney D G
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Toxicology. 1993 Jun 11;80(2-3):85-101. doi: 10.1016/0300-483x(93)90173-p.
An animal model in which the common carotid artery and the jugular vein serving one side of the brain are occluded by indwelling catheters has been used during the past few years to investigate acute carbon monoxide (CO) poisoning. This article reviews the recent research examining the pattern of changes in blood glucose concentration which results from CO exposure, and the manner in which altered glucose concentration alters neurologic outcome and mortality. At present it appears that either greatly depressed glucose or greatly elevated glucose during and/or after CO exposure increases morbidity and mortality. Cyanide (CN) poisoning, in contrast to CO, produces a different pattern of changes in blood glucose and lactate, and unlike CO, fails to slow cardiac AV conduction and ventricular repolarization. Through the use of magnetic resonance imaging and spectroscopic techniques, cerebral cortical edema and the changes in brain phosphagens have been assessed following CO poisoning in the rat. The published results as well as data from recent pilot studies are discussed in the light of our current understanding of CO toxicology.
在过去几年中，一种通过留置导管阻塞供应一侧大脑的颈总动脉和颈静脉的动物模型被用于研究急性一氧化碳（CO）中毒。本文综述了近期有关研究，这些研究考察了因接触CO而导致的血糖浓度变化模式，以及血糖浓度改变影响神经学转归和死亡率的方式。目前看来，在CO接触期间和/或之后，血糖大幅降低或大幅升高均会增加发病率和死亡率。与CO中毒不同，氰化物（CN）中毒会导致血糖和乳酸出现不同的变化模式，并且与CO不同，CN中毒不会减缓心脏房室传导和心室复极。通过使用磁共振成像和光谱技术，已对大鼠CO中毒后的大脑皮质水肿和脑磷酸肌酸的变化进行了评估。根据我们目前对CO毒理学的理解，对已发表的结果以及近期初步研究的数据进行了讨论。
