Izumi Y, Isozumi K, Fukuuchi Y
Department of Neurology, School of Medicine, Tokai University, Kanagawa, Japan.
Tokai J Exp Clin Med. 1993 Dec;18(3-6):117-22.
Cerebrovascular CO2 responsiveness, following noradrenaline (NA) infusion, was studied in the cat by continuous measurement of cerebral tissue oxygen tension (BrPO2), carbon dioxide tension (BrPCO2), pH (BrpH), and blood pressure (BP). Intravenous infusion of NA (1 microgram/kg/min) was done to stimulate the adrenergic nervous system. Inhalation of 5% CO2+air was performed for 3 minutes before, during, and after NA infusion. Cerebrovascular CO2 responsiveness was estimated from changes in BrPO2, BrPCO2, and BrpH. CO2 inhalation increased BrPO2, BrPCO2, and BP, but decreased BrpH, in the respective 3 stages. delta BrPO2 decreased significantly during NA infusion, but recovered after cessation of NA. NA infusion caused a decrease in CO2 responsiveness. This suggests that sympathetic hyperactivity can modify cerebrovascular CO2 responsiveness.
通过连续测量脑组织氧分压(BrPO₂)、二氧化碳分压(BrPCO₂)、pH值(BrpH)和血压(BP),研究了去甲肾上腺素(NA)输注后猫的脑血管二氧化碳反应性。静脉输注NA(1微克/千克/分钟)以刺激肾上腺素能神经系统。在NA输注前、期间和之后,吸入5%二氧化碳+空气3分钟。根据BrPO₂、BrPCO₂和BrpH的变化估计脑血管二氧化碳反应性。在各个阶段,吸入二氧化碳均增加了BrPO₂、BrPCO₂和BP,但降低了BrpH。在NA输注期间,ΔBrPO₂显著降低,但在停止NA后恢复。NA输注导致二氧化碳反应性降低。这表明交感神经过度活跃可改变脑血管二氧化碳反应性。