Effect of propofol on brain injury induced by intestinal ischemia-reperfusion in rats / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effects of propofol on brain injury induced by intestinal ischemia-reperfusion (I/R) in rats.Methods Forty-eight adult male Sprague-Dawley rats,weighing 250-300 g,were randomly allocated to one of 3 groups (n =16 each) using a random number tablesham operation group (group Sham),I/R group,and propofol group (group P).Intestinal I/R was produced by occlusion of the superior mesenteric artery for 90 min followed by reperfusion.In group P,propofol 50 mg/kg was injected intraperitoneally at 30 min before reperfusion,and the equal volume of fat emulsion was given in the other two groups.Blood samples were collected at 24 h of reperfusion for determination of serum tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) concentrations.The cerebral cortex and hippocampus were isolated for measurement of TNF-α and IL-1β mRNA expression (by real-time reverse transcriptase-polymerase chain reaction) and myeloperoxidase (MPO) activity (using colorimetric method).Morris water maze test was carried out at 1,3 and 5 days of reperfusion.Results Compared with group Sham,the serum TNF-α and IL-1β concentrations were significantly increased,the expression of TNF-o and IL-1β mRNA in the cerebral cortex and hippocampus was up-regulated,the MPO activity was increased,and the escape latency was prolonged,and the frequency of crossing the original platform was decreased during reperfusion in group I/R (P＜0.05).In group I/R,the concentrations of serum TNF-αand IL-1β were significantly decreased,thc cxpression of TNF-α and IL-1β mRNA in the cerebral cortex and hippocampus was down-regulated,and the escape latency was shortened,and the frequency of crossing the original platform was increased during reperfusion (P＜0.05),and no significant change was found in MPO activity in group P (P＞0.05).Conclusion Propofol reduces brain injury induced by intestinal I/R through inhibiting systemic and local inflammatory responses in rats.