Effect of inhibition of prostaglandin synthesis on renal function in laparotomized patients.
The effect of indomethacin, a prostaglandin (PG) synthetase inhibitor, on renal function was studied, and the relationship between PGE2 excretion in urine and renal function in laparotomized female patients was clarified. The PGE2 excretion rate significantly increased from 16.6 +/- 5.7 to 25.9 +/- 4.8 ng/h during surgery. This rate remained high during recovery. In patients who received 2 mg/kg of indomethacin (rectally) for postoperative analgesia following surgery, urine flow decreased from 67.8 +/- 5.4 to 42.2 +/- 6.4 ml/h 3.5-4.5 h. Para-aminohippurate clearance and creatinine clearance did not change following administration of indomethacin; however, sodium fractional excretion (FE Na) decreased significantly concomitant with depression of PGE2 excretion from 37.0 +/- 4.7 to 10.9 +/- 3.2 ng/h 3.5-4.5 h. This change in PGE2 excretion and FE Na was closely correlated (Y = 0.87 X + 13.8, r = 0.75, P less than 0.01). Plasma aldosterone levels did not change significantly after administration of indomethacin. These results suggest that PGE2 in the kidney contributes to the maintenance of sodium excretion in the post-operative period in surgical patients.
D000450:Aldosterone / Q000097:blood; D016861:Cyclooxygenase Inhibitors; D015232:Dinoprostone; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects*; D007813:Laparotomy; D008875:Middle Aged; D011188:Potassium / Q000378:metabolism; D011458:Prostaglandins E / Q000652:urine; D012964:Sodium / Q000378:metabolism
D016861:Cyclooxygenase Inhibitors; D011458:Prostaglandins E; D000450:Aldosterone; D012964:Sodium; D015232:Dinoprostone; D011188:Potassium; D007213:Indomethacin