Hemorrhage-Induced Cerebral Vasoconstriction in Dogs

Cerebrorascular responses to a 20% toJume hemorrhage were studied In chloralose-anesthetized dogs with tbe Doppler cerebral venous outflow method. Arterial Pco2, Pot2, and pH were held constant by servocontrol of ventilation. Tbe 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%. Tbe hemorrhage-Induced cerebral vasoconstriction In Group 2 was characterized by the following: pbenoxybenzamine (2 mg/kg i.v., n 3) reduced post-bemorrfaage CVR from 116% to 95% of prebemorrhage 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, sympatbetic vasoconstriction contributed approximately 5% of cCVR; following normotensive hemorrhage, it accounted for up to 20% of post-hemorrhage CVR. In combination witb previous studies, these data suggest that cerebrovascular responses to hemorrhage balance between autoregulatory vasodilatatloa and sympatbetic vasoconstriction.