GLUTAMINE KINETICS IN BURN PATIENTS COMPARISON WITH HORMONALLY INDUCED STRESS IN VOLUNTEERS

Authors
Citation
Dc. Gore et F. Jahoor, GLUTAMINE KINETICS IN BURN PATIENTS COMPARISON WITH HORMONALLY INDUCED STRESS IN VOLUNTEERS, Archives of surgery, 129(12), 1994, pp. 1318-1323
Citations number
22
Categorie Soggetti
Surgery
Journal title
ISSN journal
00040010
Volume
129
Issue
12
Year of publication
1994
Pages
1318 - 1323
Database
ISI
SICI code
0004-0010(1994)129:12<1318:GKIBPC>2.0.ZU;2-B
Abstract
Objective: To assess the acute and protracted adaptive response of per ipheral glutamine kinetics to a severe injury. Design: Comparison stud y. Setting: Clinical research center at a university-affiliated hospit al. Patients: Six severely burned men and five young healthy men. Inte rventions: The catabolic hormones epinephrine, cortisol, and glucagon were infused simultaneously into the femoral artery of five healthy vo lunteers, thus acutely simulating the hormonal milieu associated with a severe injury. Main Outcome Measures: Whole-body glutamine flux and peripheral glutamine kinetics were determined using glutamine labeled with nitrogen 15 and net balance measurements in patients 2 weeks foll owing a severe burn injury. Identical measurements were made in the he althy volunteers before and following 4 hours of catabolic hormone inf usion. Results: Whole-body glutamine flux increased to a similar exten t in both the burn patients and in volunteers following catabolic horm one infusion. In comparison with their basal kinetics, the hormonally simulated acute stress in the volunteers induced a significant efflux of glutamine from the leg by greatly increasing the rate of glutamine appearance. In contrast, burn patients had a significant decrease in t heir rate of glutamine appearance and achieved a similar net loss of g lutamine from the leg only by a compensatory decrease in peripheral gl utamine consumption. Conclusions: These findings suggest that in the a cute stress response, skeletal muscle preferentially releases glutamin e from its free intracellular pool. as this reserve becomes depleted, net glutamine efflux is maintained by decreasing its rate of muscle gl utamine utilization. These results suggest a failure of muscle to augm ent de novo glutamine synthesis and support the conclusion that glutam ine is a conditionally essential amino acid during critical illness.