Acute burn down regulates rabbit splanchnic and renal prostanoid release

• Published in: Prostaglandins, leukotrienes and essential fatty acids leukotrienes and essential fatty acids, 1995-09, Vol.53 (3), p.219-224
• Main Authors: Myers, S.I., Hernandez, R., Riva, A., Horton, J.W.
• Format: Article
• Language: English
• Subjects: 6-Ketoprostaglandin F1 alpha - blood; Acute Disease; Animals; Biological and medical sciences; Burns; Burns - physiopathology; Dinoprostone - blood; Epoprostenol - blood; Kidney - blood supply; Kinetics; Male; Medical sciences; Prostaglandins - blood; Rabbits; Splanchnic Circulation; Thromboxane B2 - blood; Traumas. Diseases due to physical agents
• ISSN: 0952-3278; 1532-2823
• DOI: 10.1016/0952-3278(95)90120-5

This study examines the hypothesis that acute thermal injury decreases renal and splanchnic vasodilator eicosanoids. Anesthetized rabbits were subjected to sham or a 25% total body surface area burn and fluid resuscitated. At 2, 4, 6, 12, and 24 h postburn the superior mesenteric and renal arteries were cannulated and perfused in vitro with their end organs with Krebs buffer (pH 7.4, 37°C). Renal and splanchnic prostaglandins (PGs) 6-keto-PGF 1α (PGI 2), and PGE 2, and thromboxane B 2 (TxB 2) release were measured by EIA at 15 min of perfusion. The major eicosanoids released were PGI 2 from the splanchnic bed and PGI 2 and PGE 2 from the kidney. Renal PGE 2 and PGI 2 and splanchnic PGI 2 release were decreased by 50% or more 12 h postburn ( p < 0.01) but were restored to sham burn levels 24 h postburn. Loss of these endogenous renal and splanchnic vasodilators 12 h postburn may contribute to ischemia of both vascular beds at this critical time period following acute burn injury.