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.

journal_name

Stroke

journal_title

Stroke

authors

Scremin OU,Rubinstein EH,Sonnenschein RR

doi

10.1161/01.str.9.2.160

subject

Has Abstract

pub_date

1978-03-01 00:00:00

pages

160-5

issue

2

eissn

0039-2499

issn

1524-4628

journal_volume

9

pub_type

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