title: Cerebrovascular CO2 reactivity: role of a cholinergic mechanism modulated by anesthesia.
abstract: 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.
mesh_terms: 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
chemical_list: D002245:Carbon Dioxide; D001285:Atropine; D010830:Physostigmine; D009609:Nitrous Oxide; D006221:Halothane