Metabolic, endocrine, and immune effects of stress hyperglycemia in a rabbit model of prolonged critical illness

被引:180
作者
Weekers, F
Giulietti, AP
Michalaki, M
Coopmans, W
Van Herck, E
Mathieu, C
Van den Berghe, G
机构
[1] Catholic Univ Louvain, Dept Intens Care Med, Burn Unit, B-3000 Louvain, Belgium
[2] Catholic Univ Louvain, Ctr Expt Surg & Anesthesiol, B-3000 Louvain, Belgium
[3] Catholic Univ Louvain, Lab Expt Med & Endocrinol, B-3000 Louvain, Belgium
关键词
D O I
10.1210/en.2003-0697
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Stress hyperglycemia is frequent in critically ill patients. The aim of this study was to investigate the effect of blood glucose control with insulin on endocrine, metabolic, and immune function in an animal model of severe injury. Seventy-two hours after alloxan injection and exogenous insulin infusion combined with continuous iv parenteral nutrition, male New Zealand White rabbits received a burn injury and were allocated to a normoglycemic (n = 17) or hyperglycemic (n = 13) group. In the normoglycemic group, blood glucose levels were kept between 3.3 and 6.1 mmol/liter by insulin infusion, whereas in the hyperglycemic group blood glucose levels were maintained at 13.8 - 16.6 mmol/liter. Blood was drawn for biochemical analysis at regular time points. At 24 and 72 h after burn injury, immune function of monocytes was assessed in vitro. Maintenance of normoglycemia with exogenous insulin after severe trauma to a large extent prevented weight loss, lactic acidosis, and hyponatremia. Furthermore, within 3 d after injury, the intervention improved phagocytosis of monocytes investigated in fresh cells by more than a mean 150% ( P = 0.006) and after 24-h incubation with or without lipopolysaccharide by more than a mean 4-fold ( P = 0.001) and 2-fold ( P = 0.05), respectively. Oxidative killing after 24-h incubation was also improved by 2-fold ( P = 0.05), but no effect on chemotaxis was detected. Concomitantly, inflammation and stress-induced growth hormone hypersecretion were suppressed. Prevention of catabolism, acidosis, excessive inflammation, and impaired innate immune function may explain previously documented beneficial effects of intensive insulin therapy on outcome of critical illness.
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页码:5329 / 5338
页数:10
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