LONG-TERM RESUSCITATION OF HEMORRHAGE REPERFUSION INJURY (H/R) STIMULATES RENAL PGE(2) RELEASE/

This study examines the hypothesis that long-term resuscitation with h yperalimentation (TPN) following acute hemorrhage/reperfusion (H/R) in jury stimulates renal release of PGE(2). Male Sprague-Dawley rats were anesthetized and subjected to sham or hemorrhage to 30 mmHg for 30 mi n followed by reperfusion. All rats were placed on TPN for 5 days, the n underwent laparotomy for in vivo renal artery and aortic blood flow for 60 min. The kidney was perfused in vitro with Krebs-Henseleit buff er at 3 ml/min (pH 7.4, 37 degrees C) and venous effluent was collecte d for analysis of PGE(2), 6-keto-PGF(1 alpha) and thromboxane B-2 by E IA. Hemorrhage/reperfusion followed by TPN for 5 days increased renal PGE(2) 2-fold and decreased in vivo renal artery blood flow by 50% com pared to the sham group. Hemorrhage/reperfusion followed by TPN did no t alter release of the other eicosanoids measured. These data suggest that the kidney has a limited capacity to maintain renal blood flow by increasing release of PGE(2) when the animal is subjected to long-ter m resuscitation with TPN following mild hemorrhage/reperfusion injury.