Baughman V L, Hoffman W E, Miletich D J, Albrecht R F
Department of Anesthesiology, Michael Reese Hospital and Medical Center, Chicago, IL 60616.
Anesthesiology. 1990 Aug;73(2):269-72. doi: 10.1097/00000542-199008000-00014.
There is controversy about whether N2O increases cerebral blood flow and cortical oxygen consumption (CMRO2) in rats. Cortical and subcortical blood flow and CMRO2 were measured in awake, unrestrained rats while awake and during 70% N2O administration using radioactive microspheres. In the awake state, cortical and subcortical blood flow were 126 +/- 10 and 98 +/- 7 ml.100 g-1.min-1, respectively, and CMRO2 (cortical) was 10.0 +/- 0.6 ml O2.100 g-1.min-1 (mean +/- SE). After 15 min of 70% N2O, cortical and subcortical blood flow increased 100% and 40%, respectively, while CMRO2 did not increase significantly. Cerebral blood flow remained increased after 60 min of N2O exposure, and CMRO2 did not change. These results show that N2O produces cerebrovasodilation in rats that is not related to a change in metabolic demand. Plasma catecholamines do not change during N2O administration, indicating that the increase in blood flow is not due to a general stress response.
关于一氧化二氮(N2O)是否会增加大鼠的脑血流量和皮质氧耗量(CMRO2)存在争议。使用放射性微球在清醒、不受约束的大鼠清醒时以及吸入70% N2O期间测量皮质和皮质下血流量及CMRO2。在清醒状态下,皮质和皮质下血流量分别为126±10和98±7 ml·100 g-1·min-1,皮质CMRO2为10.0±0.6 ml O2·100 g-1·min-1(平均值±标准误)。吸入70% N2O 15分钟后,皮质和皮质下血流量分别增加了100%和40%,而CMRO2没有显著增加。暴露于N2O 60分钟后,脑血流量仍保持增加,而CMRO2没有变化。这些结果表明,N2O在大鼠中引起脑血管舒张,这与代谢需求的变化无关。吸入N2O期间血浆儿茶酚胺没有变化,表明血流量增加不是由于一般的应激反应。