Jl. Iglesias et al., THE EFFECT OF SEQUENTIAL INJURIES ON SPLANCHNIC PERFUSION AND EICOSANOID RELEASE, The Journal of surgical research (Print), 78(2), 1998, pp. 148-154
Background. This study examines the hypothesis that sequential burn in
jury followed by intraabdominal sepsis induces significantly greater s
planchnic hypoperfusion and reduced intestinal PGI(2) release than eit
her injury independently. Materials and methods. Anesthetized Sprague-
Dawley rats were randomized to one of four groups: BURN (45% body surf
ace area scald burn) + cecal ligation and puncture (CLP); BURN alone;
CLP alone; or uninjured controls (SHAM). Twenty-four hours following i
njury, superior mesenteric artery (SMA) blood flow was measured with a
doppler flow probe. Splanchnic eicosanoid release (6-keto-PGF(1 alpha
), metabolite of PGE(2); TxB(2), metabolite of TxA(2); and PGE(2)) was
measured in mesenteric venous effluent utilizing an isolated, perfuse
d bowel preparation. Results. SMA blood flow was no different than tha
t of controls 72 h following BURN injury alone; whereas CLP alone resu
lted in a 80% reduction in splanchnic blood flow when compared with co
ntrols (P < 0.001). SMA blood flow in animals sustaining BURN + CLP wa
s 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 d
ominant eicosanoid released by the intestine with levels 10 times grea
ter than TxB(2) and nearly 50 times greater than PGE(2). CLP either al
one or when combined with BURN was associated with a 60% decrease in s
planchnic PGI(2) release when compared to controls (P < 0.05). Conclus
ions. These data suggest that moderate BURN injury in rats attenuates
the severe reduction in splanchnic perfusion associated with intraabdo
minal sepsis and that this occurs despite profound reductions in the r
elease of the endogenous splanchnic vasodilator PGI(2). (C) 1998 Acade
mic Press.