Prolonged hemorrhagic shock decreases splanchnic prostacyclin synthesis.

The effect of increasing time of hemorrhage-induced hypotension on basal splanchnic prostanoid (PG) release was examined. Male Sprague-Dawley rats were anesthetized and hemorrhaged to 30 mm Hg for 30, 60, or 120 min (SK-30, SK-60, SK-120 groups). Following shock, the superior mesenteric artery and its end organ intestine (SV + SI) was cannulated and perfused in vitro with Krebs buffer at 3 ml/min. Basal SV + SI release of 6-keto-PGF1 alpha (6-keto), PGE2, and thromboxane B2 (TxB2) was measured in the SK groups by radioimmunoassay after 15, 30, 60, 90, and 120 min of perfusion and compared to sham-operated controls (SM-30, SM-60, and SM-120 groups). 6-Keto was the major PG released from the sham SV + SI groups and was two- to sixfold higher than PGE2 or TxB2 release. Acute shock for 30 min increased SV + SI 6-keto release threefold or higher than the SM-30 group after 15-90 min of perfusion. Acute shock for 60 or 120 min lowered all PG release below SM-60 and SM-120 levels. These data confirmed our earlier study which showed that the SV + SI attempted to compensate for acute hemorrhagic shock for 30 min by increased release of prostacyclin, a potent endogenous vasodilator. The present study showed that the capacity of the SV + SI to increase endogenous prostacyclin release following hemorrhagic shock was limited by the time duration of the hypotension.