Background and Purpose: Little is known about the effects of hypothermia on cerebral autoregulation. The present study was designed to examine cerebral blood flow responses to controlled hemorrhagic hypotension in normothermic and hypothermic rats. Methods: Cortical blood flow was measured with a laser-Doppler flowmeter in halothane-anesthetized rats assigned to one of three groups: normothermic group 1 (n=8) with a pericranial temperature of ≈36.5°C or hypothermic group 2 (n=8) or group 3 (n=8) with a pericranial temperature of ≈30.5°C. In group 2, a PaCO2 of ≈40 mm Hg was maintained without correction for body temperature. To evaluate the role of PaCO2, in group 3 animals PaCO2 was kept at ≈40 mm Hg as corrected for body temperature. In all animals, the mean arterial blood pressure was reduced by hemorrhage in increments of 10 mm Hg every 2 minutes. Results: In group 1 animals, a typical autoregulatory curve was observed with cerebral blood flow first falling at or below 75% of baseline at a mean arterial pressure of 57±15 mm Hg (mean±SD). Absolute normotensive cerebral blood flow in group 2 fell to <75% of baseline at a mean arterial pressure of 73±21 mm Hg. In group 3, no evidence of autoregulation was seen. Cerebral blood flow reached values <75% of baseline at a mean arterial pressure of 82±14 mm Hg, whereas calculated cerebrovascular resistance failed to show any compensatory vasodilation as the mean arterial pressure decreased. Conclusions: Different PaCO2 management schemes used during hypothermia may have profound effects on cerebral blood flow and on autoregulation. If PaCO2 is maintained at 40 mm Hg after correction for temperature, autoregulation is abolished. If uncorrected PaCO2 is maintained at ≈40 mm Hg, some degree of autoregulation is preserved, albeit with a right-shifted "knee.".
- Cerebral blood flow