Long-term resuscitation of hemorrhage/reperfusion injury (H/R) stimulates renal PGE2 release.
This study examines the hypothesis that long-term resuscitation with hyperalimentation (TPN) following acute hemorrhage/reperfusion (H/R) injury stimulates renal release of PGE2. Male Sprague-Dawley rats were anesthetized and subjected to sham or hemorrhage to 30 mmHg for 30 min followed by reperfusion. All rats were placed on TPN for 5 days, then underwent laparotomy for in vivo renal artery and aortic blood flow for 60 min. The kidney was perfused in vitro with Krebs-Henseleit buffer at 3 ml/min (pH 7.4, 37 degrees C) and venous effluent was collected for analysis of PGE2, 6-keto-PGF1 alpha and thromboxane B2 by EIA. Hemorrhage/reperfusion followed by TPN for 5 days increased renal PGE2 2-fold and decreased in vivo renal artery blood flow by 50% compared to the sham group. Hemorrhage/reperfusion followed by TPN did not 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 PGE2 when the animal is subjected to long-term resuscitation with TPN following mild hemorrhage/reperfusion injury.
Myers
S I
SI
Department of Surgery, University of Texas Southwestern Medical Center, Dallas, USA.
Seelig
A R
AR
Turnage
R H
RH
D000818:Animals; D015232:Dinoprostone / Q000378:metabolism*; D015777:Eicosanoids / Q000378:metabolism; D006470:Hemorrhage / Q000378:metabolism*; D007668:Kidney / Q000098:blood supply / Q000378:metabolism*; D008297:Male; D008954:Models, Biological; D010289:Parenteral Nutrition, Total; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation; D015427:Reperfusion Injury / Q000378:metabolism*; D012151:Resuscitation / Q000379:methods*; D013929:Thromboxane B2 / Q000378:metabolism; D013997:Time Factors; D014665:Vasodilator Agents / Q000378:metabolism
D015777:Eicosanoids; D014665:Vasodilator Agents; D013929:Thromboxane B2; D015232:Dinoprostone