Leukotriene C4 regulation of splanchnic blood flow during ischemia.

The role of endogenous splanchnic eicosanoids in mediating splanchnic vasoconstriction induced by the leukotriene C4 (LTC4) was examined during mild hemorrhage/reperfusion injury. Male Sprague-Dawley rats were anesthetized and subjected to sham or acute hemorrhage for 30 minutes, to 30 mm Hg, followed by blood reperfusion (SK+R). The superior mesenteric artery was cannulated and removed with its end-organ intestine (SV+SI preparation) and perfused in vitro with oxygenated Krebs-Henseleit buffer. Perfusion pressure was constantly recorded. Net SV+SI release of 6-keto-PGF1 alpha, PGE2 and thromboxane B2 were analyzed by enzyme immunoassay after LTC4 stimulation. Leukotriene C4 increased perfusion pressure and decreased the ratio of 6-keto-PGF1 alpha to thromboxane release (but not PGE2 to thromboxane B2) in the sham group. Hemorrhage/reperfusion increased perfusion pressure and decreased the ratio of 6-keto-PGF1 alpha to thromboxane B2. Mild hemorrhage/reperfusion increased LTC4-induced splanchnic vasoconstriction in part by decreasing the release ratio of endogenous splanchnic PGI2 to thromboxane B2.