Chodobski A, Szmydynger-Chodobska J, Segal M B, McPherson I A
Department of Clinical and Applied Physiology, School of Medicine, Warsaw, Poland.
Prog Brain Res. 1992;91:19-22. doi: 10.1016/s0079-6123(08)62311-0.
The effect of central administration of AII on CSF formation was studied in alpha-chloralose and urethane anesthetized rabbits using the ventriculocisternal perfusion method. AII infused i.c.v. at rates of 5.5 and 55 pg/min significantly decreased CSF production by 25% and 35%, respectively. In contrast, AII when given at 5.5 ng/min did not change CSF formation. It seems that drop in CSF production observed during central administration of AII at low doses is mediated by both increased vasopressin release and activation of the sympathetic nervous system. The lack of changes in CSF formation with the highest AII dose used is not clear at present and awaits further investigation. Specific AII antagonist, saralasin, was found to significantly increase CSF production in four of five animals studied. It is suggested that in normal conditions AII may exert a tonic inhibitory effect on CSF formation.
采用脑室-脑池灌注法,在α-氯醛糖和乌拉坦麻醉的家兔中研究了中枢给予血管紧张素II(AII)对脑脊液生成的影响。以5.5和55皮克/分钟的速率脑室内注入AII分别使脑脊液生成显著减少25%和35%。相比之下,以5.5纳克/分钟给予AII时,脑脊液生成未发生变化。似乎在低剂量中枢给予AII期间观察到的脑脊液生成下降是由血管加压素释放增加和交感神经系统激活共同介导的。使用的最高AII剂量时脑脊液生成缺乏变化目前尚不清楚,有待进一步研究。在研究的五只动物中,有四只发现特异性AII拮抗剂沙拉新可显著增加脑脊液生成。提示在正常情况下,AII可能对脑脊液生成发挥紧张性抑制作用。