Effects of Dexmedetomidine on Microregional O2 Balance during Reperfusion after Focal Cerebral Ischemia

Background: This study was performed to determine whether there is an association between microregional O-2 balance and neuronal survival in cerebral ischemia-reperfusion using dexmedetomidine, an alpha(2)-adrenoreceptor agonist and a sedative. Methods: Rats were subjected to 1 hour middle cerebral artery occlusion and a 2-hour reperfusion. During reperfusion, normal saline (n = 14) or dexmedetomidine 1 mu g/kg/minute (n = 14) was infused intravenously. At 2 hours of reperfusion, regional cerebral blood flow using C-14-iodoantipyrine autoradiography, microregional arterial and venous (20-60 mm in diameter) O-2 saturation (SvO(2)) using cryomicrospectrophotometry, and the size of cortical infarction were determined. Results: Ischemia-reperfusion decreased microregional SvO(2) (52.9 +/- 3.7% vs. 61.1 +/- .6%, P < .005) with increased variation or heterogeneity (P < .0001) with similar regional cerebral blood flow and O-2 consumption. Dexmedetomidine during reperfusion decreased the heterogeneity of SvO(2) that was analyzed with an analysis of variance (P < .01) and reported as coefficient of variation (100 x standard deviation/Mean) (11.8 vs. 16.4). The number of veins with O-2 saturation less than 50% decreased with dexmedetomidine (13/80 vs. 27/81, P < .01). The percentage of cortical infarct in total cortex was smaller with dexmedetomidine (8.3 +/- 2.2% vs. 12.6 +/- 1.5%, P < .005). Conclusions: In the cerebral ischemic reperfused cortex, dexmedetomidine decreased the heterogeneity of SvO(2) and the number of small veins with low O-2 saturation suggesting improved microregional O-2 supply/consumption balance. The improvement was accompanied by the reduced size of cortical infarction.