The effects of dexmedetomidine on regional cerebral blood flow and oxygen consumption during severe hemorrhagic hypotension in rats.

BACKGROUND: We performed this study to determine how dexmedetomidine would affect regional cerebral blood flow (rCBF) and microregional O(2) consumption during nonhemorrhagic normovolemia and during severe hemorrhagic hypotension in rats.
METHODS: Forty-eight male rats were anesthetized with isoflurane and their lungs were mechanically ventilated. Half of the rats were bled to reach a mean arterial blood pressure of 40 to 45 mm Hg and were maintained at this level for at least 30 minutes before rCBF or microregional arterial oxygen saturation (Sao(2)) and venous oxygen saturation (Svo(2)) were determined. The other half were not bled and served as nonhemorrhagic controls. Half of each group was given dexmedetomidine 1 μg/kg/min IV for 45 minutes and the other half was given the same amount of normal saline infusion. The infusion started 10 minutes before blood withdrawal for the hemorrhagic groups. The rCBF was determined using (14)C-iodoantipyrine, and the microregional Sao(2) and Svo(2) were determined using cryomicrospectrophotometry at 45 minutes of infusion.
RESULTS: Dexmedetomidine decreased heart rate by 25%, but the decrease of mean arterial blood pressure was not significant. The total amount of blood withdrawn and hemoglobin were similar between the normal saline-treated and the dexmedetomidine-treated groups. In normovolemia, dexmedetomidine significantly decreased rCBF (-58%) in the lateral cortex with a similar percentage decrease (-57%) of calculated O(2) consumption. Microregional Svo(2) was similar between the normal saline-treated group (62.8% ± 1.3% [mean ± SD]) and the dexmedetomidine-treated group (60.7% ± 1.8%) despite a large difference in rCBF. Hemorrhage significantly decreased rCBF (-44%) in the lateral cortex in the normal saline-treated rats with no significant change in regional cerebrovascular resistance. In contrast, in the lateral cortex of the dexmedetomidine-treated rats, the decrease of rCBF was not significant but there was a significant decrease in regional cerebrovascular resistance. A decrease (-25%) in the O(2) consumption was observed in the lateral cortex of the normal saline-treated rats with hemorrhage, but hemorrhage did not decrease O(2) consumption in the dexmedetomidine-treated rats. Despite significantly lower rCBF (-34%) in the dexmedetomidine-treated rats, the Svo(2) was similar between the normal saline-treated (42.8% ± 2.5%) and the dexmedetomidine-treated rats (43.2% ± 2.7%).
CONCLUSIONS: Our data showed that in normovolemia, dexmedetomidine produced a proportionate decrease of rCBF and O(2) consumption. Hemorrhage decreased rCBF more than O(2) consumption. Dexmedetomidine prevented rCBF and O(2) consumption from decreasing after hemorrhage. Our data suggest that dexmedetomidine may help provide optimal O(2) supply and consumption balance during hemorrhage.