Effect of dexmedetomidine on oxidative stress responses during global cerebral ischemia-reperfusion in rats

Abstract

Objective To evaluate the effects of dexmedetomidine on the oxidative stress responses during global cerebral ischemia-reperfusion (I/R) in rats. Methods Thirty-six male Sprague-Dawley rats, weighing 250-300 g, were randomly divided into 3 groups (n=12 each) using a random number table: sham operation group (group S), global cerebral I/R group (group I/R) and dexmedetomidine group (group D). Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg). In group D, dexmedetomidine was infused at a rate of 3 μg·kg-1·h-1until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was intravenously injected immediately after onset of reperfusion.The neurological deficit score (NDS) was assessed at 24 h of reperfusion, the rats were then sacrificed, and their brains were immediately removed for determination of cell apoptosis and levels of malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT). Apoptotic rate was calculated. Results Compared with group S, NDS, apoptotic rate and MDA level were significantly increased, and SOD and CAT levels were decreased in I/R and D groups.Compared with group I/R, NDS, apoptotic rate and MDA level were significantly decreased, and SOD and CAT levels were increased in group D. Conclusion Dexmedetomidine attenuates global cerebral I/R injury through inhibiting the oxidative stress responses. Key words: Dexmedetomidine; Reperfusion injury; Brain; Oxidative stress