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Prostaglandin synthetase inhibitors are not beneficial in the hypercatabolic state of acute uremia in rats

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Research in Experimental Medicine

Summary

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, andN τ-methylhistidine (N τ-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 < 0.01) concentrations of serum urea nitrogen, creatinine, and potassium. Moreover, the urea nitrogen appearance andN τ-MH serum concentration increased (P < 0.05) significantly. Administration of indomethacin (4 mg · kg−1 b.wt./12 h i.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.

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References

  1. Baracos V, Rodemann HP, Dinarello CA, Goldberg AL (1983) Stimulation of muscle protein degradation and prostaglandin E2 release by leukocytic pyrogen (interleukin-1). N Engl J Med 308:553–558

    PubMed  Google Scholar 

  2. Butler RR, Jr, Wise WC, Haluska PV, Cook JA (1983) Gentamicin and indomethacin in the treatment of septic shock effects on prostacyclin and thromboxane A2 production. J Pharmacol Exp Ther 225:94–101

    PubMed  Google Scholar 

  3. Flügel-Link RM, Salusky JB, Jones MR, Kopple JD (1983) Protein and amino acid metabolism in posterior hemicorpus of acutely uremic rats. Am J Physiol 244 (Endocrinol Metab 7):E 615-E 623

    Google Scholar 

  4. Haverberg L, Deckelbaum L, Bilmazes C, Munro H, Young V (1975) Myofibrillar protein turnover and urinary Nτ methylhistidine output. Biochem J 152:503–510

    PubMed  Google Scholar 

  5. Heidland A, Hörl WH (1984) Contribution of proteases to hypercatabolism in acute renal failure. In: Robinson RR (ed) Nephrology. Springer, Berlin Heidelberg New York, pp 763–775

    Google Scholar 

  6. Hillgartner FB, Morin D, Hansen RJ (1982) Effect of excessive vitamine A intake on muscle protein turnover in the rat. Biochem J 202:499–508

    PubMed  Google Scholar 

  7. Hörl WH, Stepinski J, Gantert C, Hörl M, Heidland A (1981) Evidence for the participation of proteases on protein catabolism during hypercatabolic renal failure. Klin Wochenschr 59:751–759

    PubMed  Google Scholar 

  8. Huang YS, Falardeau P, Martineau A, Nestruck AC, Davignon J (1986) Effect of indomethacin treatment on prostaglandin excretion and tissue phospholipid fatty acid composition in rats bearing mammotropic pituitary tumor, MtF-F4. Prostaglandins Leukotrienes Med 23:249–252

    Google Scholar 

  9. Kopple JD (1981) Nutritional therapy in kidney failure. Nutr Rev 39:193–206

    PubMed  Google Scholar 

  10. Laidlaw SA, Zipser R, Tasaki T, Wu SHW, Kopple ID (1985) Inhibition of prostaglandin E2 (PGE2) release by indomethacin (IND) does not decrease muscle protein degradation in acutely uremic rats. Kidney Int 27:233

    Google Scholar 

  11. Li J, Wassner S (1986) Protein synthesis and degradation in skeletal muscle of chronically uremic rats. Kidney Int 29:1136–1143

    PubMed  Google Scholar 

  12. Millward DJ, Bates PC (1983) 3-Methylhistidine turnover in the whole body, and the contribution of skeletal muscle and intestine to urinary 3-methylhistidine excretion in the adult rat. Biochem J 214:607–615

    PubMed  Google Scholar 

  13. Rennie MJ, Millward DJ (1983) 3-Methylhistidine excretion and the urinary 3-methylhistidine/creatinine ratio are poor indicators of skeletal muscle protein breakdown. Clin Sci 65:217–225

    PubMed  Google Scholar 

  14. Rodemann HP, Waxman L, Goldberg AL (1982) The stimulation of protein degradation in muscle by Ca2+ is mediated by prostaglandin E2 and does not require the calcium-activated protease. J Biol Chem 257:8716–8723

    PubMed  Google Scholar 

  15. Rodemann HP, Goldberg AL (1982) Arachidonic acid, prostaglandin E2 and F2 influence rates of protein turnover in skeletal and cardiac muscle. J Biol Chem 257:1632–1638

    PubMed  Google Scholar 

  16. Schaefer RM, Weipert J, Moser M, Peter G, Heidbreder E, Hoerl WH, Heidland A (1988) Reduction of urea generation and muscle protein degradation by adrenalectomy in acutely uremic rats. Nephron 48:149–153

    PubMed  Google Scholar 

  17. Teschner M, Heidland A (1985) Nutrition in acute renal failure. Blood Purif 3:170–178

    PubMed  Google Scholar 

  18. Young VR, Alexis SD, Baliga BS, Munro H, Muecke W (1972) Metabolism of administered 3-methylhistidine, lack of muscle transfer ribonucleic acid charging and quantitative excretion as 3-methylhistidine and its N-acetyl derivate. J Biol Chem 247:3592–3600

    PubMed  Google Scholar 

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Weipert, J., Peter, G. & Heidland, A. Prostaglandin synthetase inhibitors are not beneficial in the hypercatabolic state of acute uremia in rats. Res. Exp. Med. 188, 183–187 (1988). https://doi.org/10.1007/BF01852319

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  • DOI: https://doi.org/10.1007/BF01852319

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