Cortical acetylcholine efflux with hypercapnia and nociceptive stimulation.
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 CO2 from 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.
D000109:Acetylcholine / Q000378:metabolism*; D000768:Anesthesia, General; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D002799:Cholinergic Fibers; D003655:Decerebrate State / Q000378:metabolism*; D004569:Electroencephalography; D006221:Halothane / Q000494:pharmacology; D006935:Hypercapnia / Q000378:metabolism*; D008297:Male; D009609:Nitrous Oxide / Q000494:pharmacology; D010146:Pain / Q000378:metabolism*; D011817:Rabbits
D009609:Nitrous Oxide; D000109:Acetylcholine; D006221:Halothane