To evaluate whether baseline hematocrit affects cerebral vascular reactivity to CO2, we studied the cerebral blood flow velocity in the internal carotid artery of newborn baboons, using a pulsed Doppler technique with direct imaging. Velocity responses to varying arterial CO2 tension (PaCO2) levels were first tested under baseline hematocrit (mean +/- SD, 35.9 +/- 4.7%), after hemodilution (hematocrit 20.3 +/- 2.7%), and after hemoconcentration (hematocrit 52.7 +/- 5.2%). The data were analyzed using multiple regression models, in which blood flow velocity values were the dependent variables, and PaCO2, hematocrit, and their interaction terms (product) were the independent variables. Models for the maximum systolic velocity, time-averaged mean velocity, and the end-diastolic velocity revealed a highly significant PaCO2 effect; with each mm Hg PaCO2 increase, the velocities increased between 2.9 and 3.6% (21.8-27% per 1 kPa). PaCO2 and hematocrit interaction terms were also highly significant and inversely related to velocity (negative slopes) in the maximum systolic velocity and time-averaged mean velocity models, suggesting that when the hematocrit is high, the PaCO2-induced increase in flow velocity would be attenuated, and when the hematocrit is low, such a response would be accentuated. The hematocrit effect on PaCO2 reactivity was maximal on maximum systolic velocity and least on end-diastolic velocity. Systolic velocity acceleration slope was significantly reduced when the hematocrit was high, and increased when the hematocrit was low. Based on these findings, we conclude that hematocrit is an important variable affecting the rate of kinetic energy change in the large vessels, thereby influencing cerebral vascular PaCO2 reactivity as assessed in Doppler studies.(ABSTRACT TRUNCATED AT 250 WORDS)