Differential effects of acute thermal injury on rat splanchnic and renal blood flow and prostanoid release

Abstract

This study examines the hypothesis that acute thermal injury decreases renal and splanchnic blood flow which correlates with altered endogenous vasodilator eicosanoid release. Anesthetized male Wistar rats were subjected to sham or a non-resuscitated 30% total body surface area burn. At 1, 2, 4, 8, and 24 h post-burn mean arterial pressure as well as superior mesenteric and renal artery in vivo blood flow were measured. 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 6-keto-PGF 1α (PGI 2), PGE 2, and thromboxane B 2 (TXB 2) release were measured by EIA at 15 min of perfusion. Renal and superior mesenteric artery blood flow decreased by 40% or more at 1 and 2 h post-burn despite mean arterial pressure remaining unchanged. The major eicosanoids released were PGI 2 from the splanchnic bed and PGI 2 and PGE 2 from the kidney. Splanchnic PGI 2 and TXB 2 release and renal TXB 2 increased 2–3 fold at 1 h post-burn but returned to the sham level at 2 h post-burn. By 24 h post-burn the vasodilator eicosanoids were increased in both the splanchnic and renal vascular beds. These data show that decreased renal and splanchnic blood flow was associated with increased endogenous release of the potent vasoconstrictor TXB 2. By 2 h post-burn, renal and splanchnic blood flow began returning toward the sham level as endogenous release of TXB 2 from both organs fell to sham levels. These data suggest that increased endogenous release of TXB 2 may contribute to the short-term decrease in renal and splanchnic blood flow in the immediate post-burn period and thus may contribute to ischemia of both vascular beds.