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.
journal_name
Strokejournal_title
Strokeauthors
Scremin OU,Rubinstein EH,Sonnenschein RRdoi
10.1161/01.str.9.2.160subject
Has Abstractpub_date
1978-03-01 00:00:00pages
160-5issue
2eissn
0039-2499issn
1524-4628journal_volume
9pub_type
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