P. Rothenbach et al., DOWNSTREAM EFFECTS OF SPLANCHNIC ISCHEMIA-REPERFUSION INJURY ON RENAL-FUNCTION AND EICOSANOID RELEASE, Journal of applied physiology, 83(2), 1997, pp. 530-536
This study examines the hypothesis that intestinal ischemia-reperfusio
n (I/R) injury contributes to renal dysfunction by altered renal eicos
anoid release. Anesthetized Sprague-Dawley rats underwent 60 min of sh
am or superior mesenteric artery (SMA) occlusion with 60 min of reperf
usion. The I/R groups received either allopurinol, pentoxifylline, 1-b
enzylimidazole, or carrier before SMA occlusion. In vivo renal artery
blood flow was measured by Transonic flow probes, the kidneys were the
n perfused in vitro for 30 min, and the effluent was analyzed for eico
sanoid release and renal function. Intestinal I/R caused a twofold inc
rease in the ratio of renal release of thromboxane B-2 to prostaglandi
n E-2 and to 6-ketoprostaglandin F-1 alpha compared with the sham leve
l, with a corresponding 25% decrease in renal sodium and inulin cleara
nce and renal blood flow Pentoxifylline or allopurinol pretreatment re
stored renal eicosanoid release and renal sodium and inulin clearance
to the sham level but did not alter renal blood flow. Pretreatment wit
h 1-benzylimidazole restored renal function, eicosanoid release, and r
enal blood flow to sham levels. These data suggest that severe intesti
nal I/R contributes to the downregulation of renal function. The decre
ase in renal function is due in part to toxic oxygen metabolites, whic
h occur in the milieu of altered renal eicosanoid release, reflecting
a decrease in vasodilator and an increase in vasoconstrictor eicosanoi
ds.