Prostaglandin synthetase inhibitors are not beneficial in the hypercatabolic state of acute uremia in rats.
In rats the effect of prostaglandin synthetase inhibition on the enhanced protein degradation in acute uremia was investigated. After 48 h of bilateral nephrectomy the urea nitrogen appearance, an indicator of net protein degradation, was calculated, and N tau-methylhistidine (N tau-MH) serum concentration was measured for judging myofibrillar breakdown. Also serum urea nitrogen, creatinine, and potassium serum concentrations were followed up. All bilateral nephrectomized rats showed severe uremic disturbances with increased (P less than 0.01) concentrations of serum urea nitrogen, creatinine, and potassium. Moreover, the urea nitrogen appearance and N tau-MH serum concentration increased (P less than 0.05) significantly. Administration of indomethacin (4 mg.kg-1b.wt./12 hi.p.) in bilateral nephrectomized rats did not influence the analyzed parameters significantly. Thus, we could not demonstrate a positive influence on the increased skeletal muscle degradation in acutely uremic rats by prostaglandin synthetase inhibition. These data suggest that in our model of acute uremia prostaglandins do not play a major role in the degradation of striated muscle.
D000818:Animals; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D016861:Cyclooxygenase Inhibitors; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008762:Methylhistidines / Q000097:blood; D009392:Nephrectomy; D011188:Potassium / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains; D014511:Uremia / Q000201:enzymology / Q000378:metabolism*
D016861:Cyclooxygenase Inhibitors; D008762:Methylhistidines; D003404:Creatinine; D011188:Potassium; D007213:Indomethacin