Abstract
Objective To investigate the effect of U50488H on postoperative cognitive dysfunction induced by cardiopulmonary bypass (CPB) in rats. Methods Forty-eight adult male Sprague-Dawley rats, weighing 400-450 g, were divided into 3 groups (n=16 each) using a random number table: sham operation group (group S), CPB group and CPB plus U50488H group (group U). CPB was performed for 60 min in group CPB.U50488H 1.5 mg/kg was injected into the left lateral cerebral ventricle at 30 min prior to CPB, and then CPB was performed for 60 min in group U. Eight rats in each group were selected at 1 day after CPB, and venous blood samples were collected for determination of serum S100β protein, interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations (by enzyme-linked immunosorbent assay). Then the rats were sacrificed and right hippocampi were removed for examination of the pathological changes after haematoxylin and eosin staining.Eight rats were selected from each group at 7 days after CPB for assessment of cognitive function. Results Compared with group S, the concentrations of serum S100β protein, IL-1β and TNF-α were significantly increased in group CPB, and the escape latency was prolonged, the number of crossing original platform was reduced, and the swimming distance in target quadrant and time of staying at target quadrant were shortened in CPB and U groups (P<0.05). Compared with group CPB, the concentrations of serum S100β protein, IL-1β and TNF-α were significantly decreased, the escape latency was shortened, the number of crossing original platform was increased, the swimming distance in target quadrant and time of staying at target quadrant were prolonged (P<0.05), and the pathological changes of hippocampal tissues were significantly attenuated in group U. Conclusion U50488H can mitigate the postoperative cognitive dysfunction induced by CPB in rats. Key words: Receptors, opioid, kappa; Cardiopulmonary bypass; Cognition disorders
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