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December 1994

Glutamine Kinetics in Burn Patients: Comparison With Hormonally Induced Stress in Volunteers

Author Affiliations

From the Department of Surgery, Medical College of Virginia, Richmond (Dr Gore), and the Clinical Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Tex (Dr Jahoor).

Arch Surg. 1994;129(12):1318-1323. doi:10.1001/archsurg.1994.01420360108015

Objective:  To assess the acute and protracted adaptive response of peripheral glutamine kinetics to a severe injury.

Design:  Comparison study.

Setting:  Clinical research center at a university-affiliated hospital.

Patients:  Six severely burned men and five young healthy men.

Interventions:  The catabolic hormones epinephrine, cortisol, and glucagon were infused simultaneously into the femoral artery of five healthy volunteers, 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 following a severe burn injury. Identical measurements were made in the healthy volunteers before and following 4 hours of catabolic hormone infusion.

Results:  Whole-body glutamine flux increased to a similar extent in both the burn patients and in volunteers following catabolic hormone 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 their rate of glutamine appearance and achieved a similar net loss of glutamine from the leg only by a compensatory decrease in peripheral glutamine consumption.

Conclusions:  These findings suggest that in the acute stress response, skeletal muscle preferentially releases glutamine from its free intracellular pool. As this reserve becomes depleted, net glutamine efflux is maintained by decreasing its rate of muscle glutamine utilization. These results suggest a failure of muscle to augment de novo glutamine synthesis and support the conclusion that glutamine is a conditionally essential amino acid during critical illness.(Arch Surg. 1994;129:1318-1323)

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