Growth Hormone in Critical Care Practice
The altered protein metabolism of critically ill patients is an adjustment to the specific needs of the body in a situation of strenuous demands. In short aminoacid substrates are mobilized from skeletal muscle and transported by the bloodflow to visceral organs of priority in the splanchnic area. Glutamine is a key substance as an energy substrate for enterocytes and immunocompetent cells, which can rapidly be utilized as a precursor for nucleotid synthesis when needed . In critical illness the export of glutamine from skeletal muscle is increased threefold or more . It is not clear how long a muscle is capable to maintain this elevated glutamine production. However, it is obvious that a pronounced protein depletion occurs in muscles of patients that develop multiple organ failure and consequently become long-stayers in the ICU . Muscle proteins are degraded in order to obtain aminoacid substrates for the production of glutamine. The muscle depletion that ensues has two major consequences: a decreasing ability to produce aminoacid substrates and a functional impairment. When the amounts of muscle proteins available for degradation diminishes, the production of glutamine can no longer be kept at a level to meet the demands of the proliferating tissues. A shortage of glutamine develops in tissues dependent upon a rich supply, such as the intestinal mucosa and the immunocompetent cells.
KeywordsGrowth Hormone Muscle Protein Synthesis Recombinant Human Growth Hormone Glutamine Supplementation Spec Suppl
Unable to display preview. Download preview PDF.
- 1.Hammarqvist F, Wernerman J (1994) Glutamine parenteral nutrition in critical illness. In: Vincent JL (ed) Yearbook of intensive care and emergency medicine. Springer Verlag, pp 759–770Google Scholar
- 8.Griffiths R, Jones C, Palmer A (1996) Outcome and cost of intensive care patients given glutamine-supplemented nutrition. Clin Nutr 15 [Spec suppl]:(in press)Google Scholar
- 12.Rosenfeld RG, Lamson G, Pham H et al (1991) Insulin-like growth factor binding proteins. Recent Prog Horm Res 46:99–163Google Scholar
- 13.Zap FJ, Froesch ER (1986) Insulin-like growth factors/somatomedins: Structure, secretion, biological actions and physiological role. Hormonal Reg 24:121Google Scholar
- 14.Timmins AC, Cwyfan-Hughes SC, Holly JMP et al (1996) Low circulating levels of insulinlike growth factor and alternations in binding proteins in critical illness are associated with induction of a specific protease for insulin-like growth factor binding protein 3 (IGFBP-3). Clin Intensive Care (in press)Google Scholar
- 15.Hermansson M, Wickelgren RB, Hammarqvist F (1996) Measurement of human growth hormone (GH)-receptor mRNA by a quantitative polymerase chain reaction based assay: demonstration of reduced expression after elective surgery (manuscript)Google Scholar
- 17.Tjader I, Thorne A, Tally M et al (1996) Parenteral nutrition increases IGF-1 after abdominal surgery. Clin Nutr 15 [Spec suppl] (in press)Google Scholar
- 30.Barle H, Nyberg B, Essen P et al (1996) The synthesis rate of total liver proteins and albumine determined simultaneously in vivo in man. Clin Nutr 15 [Spec suppl] (in press)Google Scholar
- 31.Barle H, Nyberg B, Essen P et al (1996) GH regulates human liver protein metabolism. Clin Nutr 15 [Spec suppl] (in press)Google Scholar
- 37.Gamrin L, Hultman E, Wernerman J (1995) Temporal development of biochemical alterations in skeletal muscle of ICU patients. Acta Anaest Scand 39[Suppl]:175Google Scholar
- 43.Roth E, Winkler S, Holzengein T et al (1992) High load of alanylglutamine in two patients with acute pancreatitis. Clin Nutr ll[Suppl]:99Google Scholar