BURN INJURY DECREASED SPLANCHNIC PGI2 RELEASE IS RESTORED BY TREATMENT WITH LAZAROID

This study examined the hypothesis that burn injury inhibits the release of splanchnic PGl2, a potent endogenous vasodilator of the splanchnic vascular bed. Male Hartley Guinea Pigs (350 grams) were anesthetized, shaved and subjected to a full thickness scald burn comprising 45% of the total body surface area (or sham burn). The animals were treated with intravenous or topical lazaroid, a 21-aminosteroid U75412E. After recovery for 24 hours, the animals were anesthetized, and the superior mesenteric artery was cannulated and removed with its intact intestine (SV+Sl). The SV+Sl was perfused in vitro with oxygenated Krebs buffer. The venous effluent was assayed for 6-keto-PGF1alpha, PGE, and thromboxane B2 by enzyme immunoassay. Acute burn injury decreased SV+Sl release of 6-keto-PGF1alpha by 57% but did not alter release of PGE, or thromboxane B2. Treatment of the animals with topical lazaroid and not intravenous lazaroid restored SV+Sl 6-keto-PGF1alpha release to control levels. These data showed that topical lazaroid therapy maintained endogenous splanchnic PGl2, release following acute burn injury. Maintaining endogenous splanchnic PGl2, release by topical lazaroid treatment may be one strategy to avoid splanchnic ischemia following acute thermal injury.