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-PGF1α (PGI2), PGE2, and thromboxane B2 (TXB2) 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 PGI2 from the splanchnic bed and PGI2 and PGE2 from the kidney. Splanchnic PGI2 and TXB2 release and renal TXB2 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 TXB2. By 2 h post-burn, renal and splanchnic blood flow began returning toward the sham level as endogenous release of TXB2 from both organs fell to sham levels. These data suggest that increased endogenous release of TXB2 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.
|Original language||English (US)|
|Number of pages||6|
|Journal||Prostaglandins, Leukotrienes and Essential Fatty Acids|
|State||Published - Dec 1995|
ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology