[The effect of intestinal ischemia/reperfusion on increased sensitivity to endotoxin and its potential mechanism]

To investigate the effect of intestinal ischemia/reperfusion injury (I/R) on increased sensitivity to endotoxin and its potential mechanism(s).

Sprague-Dawley rats underwent 45 minutes of superior mesenteric artery occlusion followed by reperfusion. Twelve hours after reperfusion, endotoxin (Escherichia coli LPS, 1.5 mg/kg) was injected intravenously and rats were killed 12 hours later for measurement of organ function parameters. Also, in vitro study was performed to determine LPS-induced tumor necrosis factor (TNF)release in whole blood.

LPS injection after I/R resulted in marked hemodynamic dysfunction and multiple organ damage(P < 0.01), while no significant or only minor changes in organ function parameters were observed in both I/R and LPS groups. In whole blood, monoclonal antibody to CD14 significantly blocked the release of TNF at low LPS concentration (< or = 10 ng/ml), and this response was dose dependent. Moreover, TNF release in LPS-stimulated whole blood obtained after I/R was inhibited to a significantly greater degree than that in baseline blood samples or sham-operation group(P < 0.05-0.01).

Splanchnic artery occlusion followed by reperfusion could lead to increased sensitivity to the subsequent LPS challenge, which may be associated with a shift toward CD14-dependent mechanism(s).