Cortical acetylcholine efflux with hypercapnia and nociceptive stimulation.
Cortical acetylcholine efflux with hypercapnia and nociceptive stimulation.
复制标题
皮质乙酰胆碱流出伴有高碳酸血症和伤害性刺激。
DOI：
10.1016/0006-8993(85)90156-8
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发表时间：
1985
期刊：
影响因子：
2.9
通讯作者：
Sonnenschein,RR
中科院分区：
文献类型：
--
作者：
Hudson,DM;Jenden,DJ;Scremin,OU;Sonnenschein,RR
在用70% N2O-30% O2麻醉的家兔，在高碳酸血症（潮末co2从4%增加到8%）和尾部轻度伤害性刺激期间，大脑皮层乙酰胆碱（ACh）的外排率翻了一番。0.7%氟烷麻醉下乙酰胆碱外排控制率低于N2O麻醉；高碳酸血症时心率升高2倍，尾刺激时心率升高4倍。在没有全身性阿托品化的情况下，乙酰胆碱外排的增加与脑电图从高电压转向低电压（“激活”）相关；全身性阿托品化后脑电图仍处于高压状态，但乙酰胆碱外排随高碳酸血症和刺激的变化不受影响。中脑横断后，乙酰胆碱外排明显下降，在高碳酸血症期间无变化。考虑到先前已知的事实，即胆碱酯酶抑制可增强高碳酸血症的脑充血，而阿托品或松解可减轻高碳酸血症的脑充血，目前的结果支持胆碱能调节脑血管系统的概念。
In rabbits anesthetized with 70% N2O-30% O2, the rate of efflux of acetylcholine (ACh) from the cerebral cortex doubled during hypercapnia (increase of end-tidal CO2from 4 to 8%), and during mild nociceptive stimulation of the tail. Under 0.7% halothane anesthesia, the control rate of ACh efflux was lower than that under N2O; the rate rose 2-fold during hypercapnia and 4-fold during tail stimulation. In the absence of systemic atropinization, increase in ACh efflux was correlated with a shift in EEG from high- to low-voltage (‘activated’);after systemic atropinization EEG remained in the high-voltage state, but the changes in ACh efflux with hypercapnia and stimulation were not affected. Following transection of the midbrain, ACh efflux was markedly depressed and did not change during hypercapnia. Taken in context with the previously known facts that the cerebral hyperemia of hypercapnia is potentiated by cholinesterase inhibition and attenuated by atropine or decerebration, the present results support the concept of a cholinergic regulation of the cerebral vasculature.