Meyer-Witting M, Helps S, Gorman D F
Department of Anaesthesia and Intensive Care, University of Adelaide, South Australia.
Anaesth Intensive Care. 1991 Aug;19(3):373-7. doi: 10.1177/0310057X9101900311.
Carbon monoxide (CO) 1% was administered to anaesthetised rabbits for 15 minutes. Despite a 28% +/- 5.8 (SEM) fall in mean arterial blood pressure during the CO exposure, cerebral blood flow increased by 236% +/- 36.5 in the left and 287% +/- 28.9 in the right cortex. Cerebrovascular resistance was reduced by 70.6% +/- 2.8 in the left and by 76.2% +/- 3 in the right cortex. These changes were accompanied by an increase in intracranial pressure, a drop in body temperature and ventilation requirement, and a metabolic acidosis. When the CO was withdrawn all these parameters returned to normal over three hours. Hence, these vascular effects are reversible and consistent with the natural history of CO intoxication in humans. Carboxyhaemoglobin levels correlated well with hemispheric cerebral blood flow (r = 0.90; r = 0.98) and cerebrovascular resistance (r = 0.87; r = 0.97).
将1%的一氧化碳（CO）给予麻醉的兔子，持续15分钟。尽管在CO暴露期间平均动脉血压下降了28%±5.8（标准误），但左侧大脑皮层的脑血流量增加了236%±36.5，右侧增加了287%±28.9。左侧大脑皮层的脑血管阻力降低了70.6%±2.8，右侧降低了76.2%±3。这些变化伴随着颅内压升高、体温下降、通气需求降低以及代谢性酸中毒。当停止给予CO后，所有这些参数在三小时内恢复正常。因此，这些血管效应是可逆的，并且与人类CO中毒的自然病程一致。碳氧血红蛋白水平与半球脑血流量（r = 0.90；r = 0.98）和脑血管阻力（r = 0.87；r = 0.97）密切相关。
