Penney D G
Wayne State Univ. School of Med, Detroit, MI 48201.
Med Hypotheses. 1988 Nov;27(3):241-4. doi: 10.1016/0306-9877(88)90151-x.
It is hypothesized that hyperglycemia naturally induced by stress and/or produced by intravenous trauma therapy adversely effects neurologic outcome following acute severe carbon monoxide poisoning, and the higher the blood glucose the greater the degree of brain dysfunction. Increased availability of glucose presumably increases cerebral glycolytic flux, and elevates intracellular and interstitial lactate level, which in turn induces acidosis and edema, resulting in brain damage. In a retrospective study of blood glucose and other data obtained from patients upon hospital admission for CO poisoning, a mean value of 409 mg/dL was associated with "brain death", a value of 215 mg/dL with "minimal to substantial brain damage," and a value of 165 mg/dL with "normal" recovery.
据推测，由应激自然诱发和/或静脉创伤治疗产生的高血糖会对急性重度一氧化碳中毒后的神经学预后产生不利影响，且血糖越高，脑功能障碍程度越严重。葡萄糖可用性增加可能会增加脑糖酵解通量，并提高细胞内和细胞间乳酸水平，进而引发酸中毒和水肿，导致脑损伤。在一项对一氧化碳中毒入院患者的血糖及其他数据的回顾性研究中，血糖平均值为409毫克/分升与“脑死亡”相关，215毫克/分升与“轻度至重度脑损伤”相关，165毫克/分升与“正常”恢复相关。
