WHOLE-BODY METABOLIC RESPONSES TO BRAIN TRAUMA IN THE RAT

Increases in metabolic rate reported in head-injured patients can cont ribute to increases in respiratory demand, raised body temperature, an d host body wasting (cachexia). The objective of the present study was to quantify the metabolic responses to brain trauma in the rat and in vestigate the underlying mechanisms. Lateral fluid-percussion (FP) inj ury (applied cortical pressure 1.6-1.8 atm) in the rat resulted in con sistent and reproducible cortical brain lesions (44 +/- 6 mm(3)). Body weight and food intake were reduced significantly 24 h after brain tr auma compared to sham-operated (7 and 49%, p < 0.01) and control anima ls (14 and 65%, p < 0.001), respectively. Resting oxygen consumption ( (V) over dot O-2, measured at 24 degrees C) was increased significantl y, by 9-16% above sham-operated, and 14-26% above control animals for 2-7 h after brain trauma (p < 0.05), but (V) over dot O-2 was not rais ed thereafter (24-72 h) and colonic temperature was not changed. Raisi ng the ambient temperature from 24 degrees C to 28 degrees C significa ntly reduced the hypermetabolism of brain-injured rats compared to sha m-operated controls. Injection of the beta-adrenoceptor antagonist pro pranolol (10 mg/kg, i.p.) completely abolished the rise in metabolic r ate of brain-injured rats, and reduced significantly the rise in metab olic rate of the sham-operated animals (26%, p < 0.01 and 11%, p < 0.0 5; respectively). Systemic injection of the cyclo-oxygenase inhibitor indomethacin (1 mg/kg, i.p.) significantly attenuated (by 11%, p < 0.0 1), but did not completely abolish the hypermetabolism of brain-injure d animals. Lateral FP injury in the rat causes a significant cachexia. Weight loss is due to hypophagia, and an increase in energy expenditu re, which is mediated by sympathetic activation of thermogenesis and i n part by prostaglandins.