Ekström-Jodal B, Larsson L E
Crit Care Med. 1982 Jun;10(6):375-7. doi: 10.1097/00003246-198206000-00008.
Experimental endotoxic shock in normocapnic dogs decreases cerebral blood flow (CBF) and increases cerebral metabolic rate of oxygen (CMRO2). In 6 animals, an iv injection of 1.0-1.5 mg/kg of Escherichia coli endotoxin was followed by iv infusion of dopamine HCI at a rate of 3-24 Micrograms/kg . min. Doses of only 5 micrograms/kg . min maximally increased both CBF and CMRO2. There were no significant changes in cardiac output and whole body oxygen consumption. Mean aortic pressure and mean pulmonary artery pressure increased slightly after doses of 20 micrograms/kg . min. Results indicate that damage to the blood-brain barrier (BBB) after endotoxin administration allowed circulating monoamines to directly influence cerebral metabolisms.
正常碳酸血症犬的实验性内毒素休克会降低脑血流量(CBF)并增加脑氧代谢率(CMRO2)。在6只动物中,静脉注射1.0 - 1.5mg/kg的大肠杆菌内毒素后,接着以3 - 24微克/千克·分钟的速率静脉输注盐酸多巴胺。仅5微克/千克·分钟的剂量就能最大程度地增加CBF和CMRO2。心输出量和全身氧消耗无显著变化。剂量为20微克/千克·分钟后,平均主动脉压和平均肺动脉压略有升高。结果表明,内毒素给药后血脑屏障(BBB)受损,使得循环中的单胺类物质能够直接影响脑代谢。