Acute burn down regulates rabbit splanchnic and renal prostanoid release.
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 degrees C). Renal and splanchnic prostaglandins (PGs) 6-keto-PGF1 alpha (PGI2), and PGE2, and thromboxane B2 (TxB2) release were measured by EIA at 15 min of perfusion. The major eicosanoids released were PGI2 from the splanchnic bed and PGI2 and PGE2 from the kidney. Renal PGE2 and PGI2 and splanchnic PGI2 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.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000208:Acute Disease; D000818:Animals; D002056:Burns / Q000503:physiopathology*; D015232:Dinoprostone / Q000097:blood; D011464:Epoprostenol / Q000097:blood; D007668:Kidney / Q000098:blood supply*; D007700:Kinetics; D008297:Male; D011453:Prostaglandins / Q000097:blood*; D011817:Rabbits; D013152:Splanchnic Circulation; D013929:Thromboxane B2 / Q000097:blood
D011453:Prostaglandins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D015232:Dinoprostone