Cerebral reactive oxygen species assessed by electron spin resonance spectroscopy in the initial stage of ischemia-reperfusion are not associated with hypothermic neuroprotection.

Using an in vivo L-band electron spin resonance (ESR) system, we determined changes in reactive oxygen species (ROS) levels during the early stage (within 60 minutes) of global cerebral ischemia-reperfusion (IR) under normothermic and hypothermic conditions in rats. To confirm the neuroprotective role of hypothermia in this IR model, we immunohistochemically evaluated the levels of active caspase-3 in the hippocampal CA1 sector. ROS levels increased within the first 15 minutes following IR under both normothermic and hypothermic conditions; however, the ROS levels did not differ significantly between normothermic and hypothermic conditions. In the later periods of IR, there were no significant changes in ROS levels for either normothermic or hypothermic conditions relative to the control. As expected, normothermia increased the number of active caspase-3 immunoreactive nuclei in the IR model. However, this induction was prevented by hypothermia. These results suggest that the neuroprotective role of hypothermia does not correlate with the early ROS-induced oxidative stress following IR as measured by ESR.