Matsuoka M, Igisu H, Tanaka I, Hori H, Koga M
Department of Environmental Toxicology, Institute of Industrial Ecological Sciences, Kitakyushu, Japan.
Toxicol Lett. 1994 Aug;73(2):135-43. doi: 10.1016/0378-4274(94)90103-1.
Hypoglycemia and hyperglycemia were induced in mice by fasting and by injecting with glucose, respectively. These and normally fed (normoglycemic) animals were exposed to 0.5% carbon monoxide (CO) for 10 min. This altered concentrations of energy metabolites in the brain, including decreases in phosphocreatine (PCr) and increases in creatine and lactate. The only difference between normoglycemic and hypoglycemic mice was lower lactate in the latter. In hyperglycemic mice, PCr and ATP were better preserved during CO exposure and lactate was lower than in normoglycemic mice. Blood glucose concentrations correlated well with glucose but not with lactate in the brain. Thus, moderate hypo- or hyperglycemia seems not to exacerbate CO-induced alterations of brain energy metabolism.
分别通过禁食和注射葡萄糖在小鼠中诱导低血糖和高血糖。将这些小鼠以及正常喂食（血糖正常）的动物暴露于0.5%的一氧化碳（CO）中10分钟。这改变了大脑中能量代谢物的浓度，包括磷酸肌酸（PCr）减少以及肌酸和乳酸增加。血糖正常和低血糖小鼠之间的唯一差异是后者的乳酸含量较低。在高血糖小鼠中，CO暴露期间PCr和ATP得到更好的保存，并且乳酸含量低于血糖正常的小鼠。血糖浓度与大脑中的葡萄糖相关性良好，但与乳酸无关。因此，中度低血糖或高血糖似乎不会加剧CO诱导的脑能量代谢改变。
