Moderate hypothermia suppresses jugular venous superoxide anion radical, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats

The aim of this study was to assess the effect of moderate hypothermia (MH) on generation of jugular venous superoxide radical (O-2(-)), oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion (FBI/R) rats Twenty-one Wistar rats were allocated to a control group (n=7, 37 degrees C), a pre-MH group (n=7, 32 degrees C before ischemia), and a post-MH group (n= 7, 32 degrees C after reperfusion) MH was induced before induction of ischemia in the pre-MH group and just after reperfusion. in the post-MH group Forebrain ischemia was induced by occlusion of bilateral common carotid arteries with hemorrhagic hypotension for 10 min, followed by reperfusion. O-2(-) in the jugular vein was measured from the produced current using a novel O-2(-) sensor The O-2(-) current showed a gradual increase during forebrain ischemia in the control and post-MH groups but was attenuated in the pre-MH group Following reperfusion, the current showed a marked increase in the control group but was strongly attenuated in the pre- and post-MH groups Concentrations of malondialdehyde, high-mobility group box 1 (HMGB1) protein, and intercellular adhesion molecule-1 (ICAM-1) in the brain and plasma 120 min after reperfusion in the pre- and post-MH groups were significantly lower than those in the control group, except for plasma HMGB1 in the post-MH group In conclusion, MH suppressed O-2(-) measured in the jugular vein, oxidative stress, early inflammation, and endothelial injury in FBI/R rats (C) 2009 Elsevier B V All rights reserved