The effect of sequential injuries on splanchnic perfusion and eicosanoid release.

BACKGROUND

This study examines the hypothesis that sequential burn injury followed by intraabdominal sepsis induces significantly greater splanchnic hypoperfusion and reduced intestinal PGI2 release than either injury independently.

MATERIALS AND METHODS

Anesthetized Sprague-Dawley rats were randomized to one of four groups: BURN (45% body surface area scald burn) + cecal ligation and puncture (CLP); BURN alone; CLP alone; or uninjured controls (SHAM). Twenty-four hours following injury, superior mesenteric artery (SMA) blood flow was measured with a doppler flow probe. Splanchnic eicosanoid release (6-keto-PGF1alpha, metabolite of PGE2; TxB2, metabolite of TxA2; and PGE2) was measured in mesenteric venous effluent utilizing an isolated, perfused bowel preparation.

RESULTS

SMA blood flow was no different than that of controls 72 h following BURN injury alone; whereas CLP alone resulted in a 80% reduction in splanchnic blood flow when compared with controls (P < 0.001). SMA blood flow in animals sustaining BURN + CLP was only modestly reduced from controls (P = 0.04) and 3.6 times greater than that of animals sustaining CLP alone (P < 0.001). PGI2 was the dominant eicosanoid released by the intestine with levels 10 times greater than TxB2 and nearly 50 times greater than PGE2. CLP either alone or when combined with BURN was associated with a 60% decrease in splanchnic PGI2 release when compared to controls (P < 0.05).

CONCLUSIONS

These data suggest that moderate BURN injury in rats attenuates the severe reduction in splanchnic perfusion associated with intraabdominal sepsis and that this occurs despite profound reductions in the release of the endogenous splanchnic vasodilator PGI2.