Urinary excretion of prostaglandin E following the administration of furosemide and indomethacin to sick low-birth-weight infants.
Urinary excretion of prostaglandin E was measured in seven sick low-birth-weight infants. Four had severe hyaline membrane disease and one had chronic bronchopulmonary dysplasia; all received furosemide. Two infants had patent ductus arteriosus and received indomethacin. Following administration of furosemide, urine volume and the excretion rates of sodium and calcium were significantly increased; such changes were not seen following the administration of indomethacin. Prostaglandin E excretion rate was increased from 0.4 +/- 0.04 to 1.3 +/- 0.2 ng/mg Cr (mean +/- SEM) following administration of furosemide, but decreased in two patients following administration of indomethacin. The present results demonstrate that furosemide enhances urinary excretion of prostaglandin E by mechanisms which may reflect an increase in prostaglandin synthesis, a decrease in prostaglandin renal metabolism, or both. Indomethacin, which is a prostaglandin synthetase inhibitor, decreases the urinary excretion of prostaglandin E. These observations suggest that furosemide therapy in patients receiving indomethacin may be ineffective.
D002118:Calcium / Q000652:urine; D004336:Drug Antagonism; D004374:Ductus Arteriosus, Patent / Q000652:urine; D005260:Female; D005665:Furosemide / Q000494:pharmacology*; D006801:Humans; D006819:Hyaline Membrane Disease / Q000652:urine; D007213:Indomethacin / Q000494:pharmacology*; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000652:urine*; D008297:Male; D011458:Prostaglandins E / Q000652:urine*; D012964:Sodium / Q000652:urine
D011458:Prostaglandins E; D005665:Furosemide; D012964:Sodium; D002118:Calcium; D007213:Indomethacin