Stroke, Vol 11, 190-197, Copyright © 1980 by American Heart Association
WJ Pearce and LG D'Alecy
Cerebrovascular responses to a 20% volume hemorrhage were studied in
chloralose-anesthetized dogs with the Doppler cerebral venous outflow
method. Arterial PCO2, PO2, and pH were held constant by servocontrol of
ventilation. The experimental results were divided into 2 groups as
determined by the spontaneous responses of mean arterial pressure (MAP) to
hemorrhage. In Group 1 (n = 11), steady state MAP decreased 25%, cerebral
blood flow (CBF) decreased 15%, and cerebrovascular resistance (CVR)
decreased 13% (autoregulatory vasodilatation). In group 2 (n = 23), MAP
changed less than 10 mm Hg, CBF decreased 13%, and CVR increased 15%. The
hemorrhage-induced cerebral vasoconstriction in Group 2 was characterized
by the following: phenoxybenzamine (2 mg/kg i.v., n = 3) reduced
post-hemorrhage CVR from 116% to 95% of prehemorrhage CVR (cCVR);
phentolamine (2 mg/kg i.v., n = 5) reduced post-hemorrhage CVR from 114% to
91% of cCVR; and verified local anesthetization of both superior cervical
ganglia (n = 5) reduced post- hemorrhage CVR from 116% to 94% of cCVR. Thus
in Group 2, sympathetic vasoconstriction contributed approximately 5% of
cCVR; following normotensive hemorrhage, it accounted for up to 20% of
post-hemorrhage CVR. In combination with prevous studies, these data
suggest that cerebrovascular responses to hemorrhage balance between
autoregulatory vasodilatation and sympathetic vasoconstriction.
ARTICLES
Hemorrhage-induced cerebral vasoconstriction in dogs
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