Growth hormone does not prevent corticosteroid-induced changes in rat diaphragm structure and function. Petrof, Basil J., Stewart B. Gottfried, Joseph Eby, John Lamanca, and Sanford Levine. Royal Victoria Hospital and Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada; Montreal General Hospital and Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada; Veterans Administration Medical Center, Medical College of Pennsylvania, Philadelphia, PA.
APStracts 2:0309A, 1995.
Recent studies in animal models and humans have shown that large doses of corticosteroids can cause atrophy and weakness of the diaphragm. The present study tested the hypothesis that growth hormone (GH), an anabolic agent, could prevent the abnormalities of diaphragm structure and function associated with short-term administration of the corticosteroid, triamcinolone (TR), in the adult rat. During a 10-d period, male rats (n=33) were equally assigned to 3 groups: control (CTL), TR (1 mg/kg/d IM), and TR + GH (2 mg/kg/d IM). Food consumption was matched among the 3 groups. Diaphragm weight was significantly reduced in the TR and TR-GH animals in comparison to CTL, but there was no difference in the diaphragm weight/body weight ratio among groups. Immunohistochemical analysis (using myosin heavy chain isoform-specific antibodies) of type I, IIa, and IIx/b fiber types showed no difference in fiber type proportions among the 3 groups. However, in TR rats there was a significant reduction in the contribution of type IIx/b fibers to total diaphragm cross-sectional area due to marked atrophy (approx. 42% decrease in mean fiber cross -sectional area) of type IIx/b fibers. There was no significant reversal of TR-induced type IIx/b fiber atrophy by concomitant GH administration. TR and TR-GH groups both exhibited enhanced in vitro fatigue resistance, whereas maximal specific force measurements (twitch and tetanus) revealed no differences among the 3 experimental groups. We conclude that TR administration results in significant diaphragm wasting with a predominance of type IIx/b fiber atrophy, as well as increased resistance to fatigue in vitro. GH did not effectively prevent these corticosteroid-induced effects, possibly as a result of the reduced nutritional intake associated with TR administration. Future studies should be aimed at determining whether hyperalimentation during GH therapy is capable of enhancing GH effects on the diaphragm in the setting of corticosteroid therapy. 

Received 2 March 1995; accepted in final form 29 June 1995.
APS Manuscript Number A235-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.