A Program for the Study of Skeletal Muscle Catabolism Following Physical Trauma
Abstract
Following injury or infection there is accelerated net breakdown of skeletal muscle protein associated with negative nitrogen balance. A variety of factors influence this response, including food intake, inactivity and the hormonal environment. In studies that control for food intake and exercise, infusion of the catabolic hormones causes negative nitrogen balance but does not account for the accelerated proteolysis that occurs following moderate to severe injury. The recent recognition that injured tissue or invasive infection stimulates the production of a variety of cytokines has caused a variety of investigators to hypothesize that these mediators may serve as the signal to accelerate skeletal muscle proteolysis. Some of the initial in vitro studies have suggested that increased skeletal muscle protein breakdown may be simulated by activation of the cyclooxygenase pathway. Others have presented data which demonstrates that proteolysis may continue even when prostinoid mechanisms are not activated. Infusion of Prostaglandin E2 (PGE2) into the single hind leg of the dog failed to stimulate the increased release of amino acids. Additional animals underwent lumbar sympathectomy and then sympathetic nerve stimulation. Following sympathectomy, leg blood flow increased, and with stimulation leg blood flow returned toward control values. Glucose Flux did not change in either leg throughout the study and was similar in both hind limbs. Amino acid analysis is presently in process.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 15, 1989
- Accession Number
- ADA207983
Entities
People
- Douglas W. Wilmore
Organizations
- Brigham and Women's Hospital