In vivo injection of isoproterenol (IPR) (4 mg/kg) in normal rats caused fat cell adenylate cyclase to become desensitized to stimulation by IPR in vitro. In contrast, adenylate cyclase from tissues of burn-injured rats (20% body surface, full-thickness scald) remained fully responsive to stimulation by IPR for several days after injury even though catecholamine excretion was elevated more than twofold. Furthermore, fat cell adenylate cyclase from burn-injured animals was not desensitized after acute in vivo IPR injections, whereas adenylate cyclase from the shams did become desensitized after acute IPR injections. To determine whether the apparent resistance to desensitization in burn-injured rats might be an adaptation to the chronic elevation of catecholamines that follows burn injury, two other rat models in which catecholamines are chronically elevated were studied: one was produced by a twice daily schedule of IPR (1 mg/kg) injections for 3 weeks; the other by 3 weeks’ cold exposure (0-4°C). As had been observed in burn injury, adenylate cyclase remained fully responsive to IPR in both models, and adenylate cyclase from the cold-acclimated rats was resistant to desensitization by acute injections of IPR. It therefore seems likely that chronic elevations of catecholamines evoke regulatory mechanisms in target cells to circumvent the desensitization which would otherwise occur consequent to acute exposures to catecholamines. In burn injury this may result in an inadvertent adaptation which contributes to hypermetabolism.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Trauma - Injury, Infection and Critical Care|
|State||Published - Nov 1979|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine