Amrinone prevents muscle protein wasting during chronic sepsis
C. V. Jurasinski, L. Kilpatrick and T. C. Vary Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey 17033. The time course for the effects of sepsis on rates of protein synthesis, RNA contents, and translational efficiencies was measured in mixed muscle...
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Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 1995-03, Vol.268 (3), p.E491-E500 |
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Zusammenfassung: | C. V. Jurasinski, L. Kilpatrick and T. C. Vary
Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey 17033.
The time course for the effects of sepsis on rates of protein synthesis,
RNA contents, and translational efficiencies was measured in mixed muscles
of rat hindlimb perfused in vitro 3, 5, and 10 days after induction of
sepsis. Furthermore, the effect of daily injections of amrinone (5
mg.kg-1.day-1) on muscle protein synthesis was investigated. On day 3 of
sepsis, decreased rates of protein synthesis in muscle from untreated
septic animals or septic rats treated with amrinone resulted from a reduced
food intake. When food intake became normalized to control after 5 days,
rates of protein synthesis in untreated septic rats remained depressed.
Treatment of septic animals with amrinone for 5 days prevented the
sepsis-induced inhibition of protein synthesis by abolishing the inhibition
of peptide-chain initiation and restoring translational efficiency to
control values. In contrast, amrinone treatment of control rats for 5 days
did not cause an accretion of muscle protein or augment protein synthesis.
Ten days after induction of sepsis, there were no differences in rates of
protein synthesis, RNA content, or translational efficiency in septic
animals compared with control or amrinone-treated septic rats. Thus,
amrinone prevented the sepsis-induced abnormalities in skeletal muscle
protein synthesis. |
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ISSN: | 0193-1849 0002-9513 1522-1555 |
DOI: | 10.1152/ajpendo.1995.268.3.E491 |