Cerebrovascular CO2 reactivity: role of a cholinergic mechanism modulated by anesthesia.
Cerebral cortical blood flow was measured in rabbits with the hydrogen clearance technique. The reactivity to CO2, tested by changing the end tidal CO2 (ETCO2) in steps from 2 to 6 volumes %, was highly dependent on the kind of anesthesia, being greatest under halothane and least under nitrous oxide. Reactivity to CO2 in halothane-anesthetized animals also depended on arterial blood pressure, being greatest when pressure was below 70 mm Hg. Intravenous atropine blocked the increase in reactivity in halothane-anesthetized animals at low blood pressures. Conversely, intravenous eserine (physostigmine) greatly increased the reactivity to CO2 in nitrous oxide-anesthetized animals. Precollicular decerebration considerably decreased CO2 reactivity of halothane-anesthetized rabbits, while partial brain stem lesions that spared midline structures had no effect on CO2 reactivity. It is concluded that a central neurogenic mechanism with a cholinergic link may be responsible, at least in part, for the cerebrovascular effect of CO2. Moreover, the cerebrovascular effects of halothane may result from stimulation of the same system.
D000758:Anesthesia; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D002799:Cholinergic Fibers / Q000187:drug effects*; D003714:Denervation; D006221:Halothane; D008297:Male; D009609:Nitrous Oxide; D010830:Physostigmine / Q000494:pharmacology; D011817:Rabbits
D002245:Carbon Dioxide; D001285:Atropine; D010830:Physostigmine; D009609:Nitrous Oxide; D006221:Halothane