Hemorrhage-induced cerebral vasoconstriction in dogs.

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.