Congestion preconditioning protects against intestinal mucosal hyperpermeability induced by congestion-reperfusion injury in rats

AIM:To investigate the effects of congestion preconditioning on intestinal barrier dysfunction caused by portal occlusion in rats. METHODS:Sprague-Dawley rats were divided into three groups:congestion-reperfusion group(CR group) ,congestion preconditioning group(CP group) and sham operation group(SO group) .In the CR group,portal vein flow was occluded using a micro-clamp for 45 min and then unclamped by removing the micro-clamp.In the CP group,the portal vein was clamped for 5 min and then unclamped for 5 min,followed by one repeat of this procedure before portal vein flow occlusion for 45 min.In the SO group,all the procedures were conducted except for the clamping of the portal vein.Portal blood samples were collected at baseline,12 h and 24 h after the portal procedure for measurement of plasma endotoxin and TNF-αconcentrations. Meanwhile,the intestine was loaded with 5 mL FITC-dextran 4400(FD4,0.2%) .One hour later. portal blood samples were taken for detection of intestinal mucosal permeability by measuring the appearance of fluorescent probe FD4 in portal plasma. RESULTS:The concentrations of FD4,endotoxin and TNF-αin portal plasma in the CR group were significantly higher than those in the SO group(24 h:0.621 mg/L±0.074 mg/L vs 0.107 mg/L±0.015 mg/L,P<0.01;0.636 EU/mL±0.064 EU/mL vs 0.056 EU/mL±0.019 EU/mL,P<0.01;107.14 ng/L±15.71 ng/L vs 11.98 ng/L±3.15 ng/L,P<0.01) .Plasma endotoxin concentration was positively correlated with FD4 level in portal plasma(r=0.9118,P< 0.01) .The levels of FD4,endotoxin and TNF-α in portal plasma in the CP group were remarkably attenuated compared with those in the CR group(24 h:0.391 mg/L±0.070 mg/L vs 0.621 mg/L±0.074 mg/L,P<0.01;0.452 EU/mL± 0.048 EU/mL vs 0.636 EU/mL±0.064 EU/mL,P<0.01;73.38 ng/L±5.37 ng/L vs 107.14 ng/L ±15.71 ng/L,P<0.01) . CONCLUSION:Congestion preconditioning has a protective effect against intestinal mucosal hyperpermeability induced by congestion-reperfusion injury and could therefore alleviate endotoxemia and systemic inflammatory reaction.