Postischemic hypothermia inhibits the generation of hydroxyl radical following transient forebrain ischemia in rats

• Published in: Japanese Journal of Stroke Vol. 26; no. 4; pp. 498 - 502
• Main Author: Horiguchi, Takashi
• Format: Journal Article
• Language: Japanese
• Published: The Japan Stroke Society 2004
• Subjects: Free radical; Neuroprotection; Reperfusion; Temperature; Xanthine
• ISSN: 0912-0726; 1883-1923
• DOI: 10.3995/jstroke.26.498

In this study we investigated the effect of postischemic hypothermia on ROS production following transient forebrain ischemia using an in vivo microdialysis technique. Forebrain ischemia was induced by bilateral carotid artery occlusion combined with hemorrhagic hypotension for 20 minutes in male Wistar rats. The body temperature was kept at 37°C during ischemia and controlled at either 32°C or 37°C after reperfusion. The amount of hydroxyl radical produced in striatum was evaluated by measurement of 2, 3-and 2, 5-dihydroxybenzoic acid (DHBA), which is generated by salicylate hydroxylation. We also measured the extracellular concentration of xanthine and striatal blood flow by the hydrogen clearance technique. In animals whose postischemic body temperature was maintained at 37°C, the levels of 2, 3-and 2, 5-DHBA significantly increased after reperfusion. The peak levels of 2, 3-and 2, 5-DHBA were 2.9-fold 2.7-fold increase above the corresponding baseline values, respectively. Postischemic hypothermia completely inhibited the hydroxyl radical formation. Likewise, xanthine formation was also inhibited by postischemic hypothermia. In contrast, striatal cerebral blood flow was not altered by temperature modulation during reperfusion. These results suggest that inhibition of ROS production accompanied with suppression of xanthine formation is implicated in the neuroprotection of postischemic hypothermia.