Abstract
Urinary excretion of prostaglandin E was measured in seven sick low birthweight infants. Four had severe hyaline membrane disease, one had chronic bronchopulmonary dysplasia and all received furosemide. Two infants suffered from patent ductus arteriosus and received indomethacin. Urinary volume and the excretion of sodium, calcium and prostaglandin E were determined in these infants before and after the administration of these drugs. Following furosemide administration, 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 furosemide administration but decreased from 1.0 to 0.4 (mean) ng/mg Cr following indomethacin administration. The mechanism(s) by which furosemide enhances urinary excretion of prostaglandin E may be an increase in prostaglandin synthesis, a decrease in their renal metabolism or both. However, indomethacin which is a prostaglandin synthetase inhibitor, decreases the urinary excretion of prostaglandin E in a dose-dependent fashion. These observations suggest the possibility that in patients receiving indomethacin furosemide therapy may be ineffective.
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Friedman, Z., Demers, L., Uhrmann, S. et al. 103 URINARY EXCRETION OF PROSTAGLANDIN E FOLLOWING THE ADMINISTRATION OF FUROSEMIDE AND INDOMETHACIN TO SICK LOW BIRTHUEIGHT INFANTS. Pediatr Res 12 (Suppl 4), 381 (1978). https://doi.org/10.1203/00006450-197804001-00108
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DOI: https://doi.org/10.1203/00006450-197804001-00108
