Effect of hemorrhagic shock on renal release of prostaglandin E.
The effect of hemorrhage and reinfusion on renal release of prostaglandin E (PGE), arterial [PGE], mixed-venous [PGE], and renal function was observed in anesthetized dogs. Following hemorrhage to 60 mmHg arterial pressure, arterial [PGE] rose significantly from 405 to 740 pg/ml. Renal release of PGE remained near control (8 ng/min), as renal blood flow (RBF) decreased from 4.7 to 2.2 ng/min per gram kidney weight (KW). Mixed-venous [PGE] remained near the control value (960 pg/ml). Reinfusion of shed blood restored RBF to 4.0 ml/min per KW. Renal release of PGE rose significantly to 190 ng/min. Arterial [PGE] remained elevated, but mixed-venous [PGE] was not significantly different from control. Indomethacin, a prostaglandin synthesis inhibitor, caused a significant decrease in renal release of PGE. Arterial [PGE] remained elevated following treatment. The inhibition of PGE release from the kidney by indomethacin indicates that increased renal release of PGE following reinfusion is the result of accelerated PGE synthesis. The data suggest that the elevated arterial [PGE] may be the result of alteration of the handling of PGE by the lung.
D000618:Aminohippuric Acids; D000818:Animals; D001794:Blood Pressure; D002118:Calcium / Q000097:blood; D004285:Dogs; D007022:Hypotension / Q000503:physiopathology; D007213:Indomethacin / Q000494:pharmacology; D007444:Inulin; D007668:Kidney / Q000378:metabolism; D008297:Male; D010710:Phosphates / Q000097:blood; D011458:Prostaglandins E / Q000097:blood / Q000378:metabolism*; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D012964:Sodium / Q000097:blood
D000618:Aminohippuric Acids; D010710:Phosphates; D011458:Prostaglandins E; D007444:Inulin; D012964:Sodium; D002118:Calcium; D007213:Indomethacin