Impaired glucose flow in burned patients with gram-negative sepsis.

Fifteen thermally injured patients with positive blood stream cultures for gram-negative organisms demonstrated a decreased mass flow of glucose through the glucose space when compared with 17 patients without sepsis studied at a comparable time after injury. Amino acid concentrations determined in ten burned patients with sepsis and nine burned patients without sepsis revealed an increase in the gluconeogenic precursors alanine, glycine, methionine and phenylalanine in those patients with sepsis. The administration of alanine consistently increased serum glucose in seven patients without sepsis but exerted no effect on glucose concentrations in six person with sepsis.

Carbohydrate metabolism in trauma.

During the initial shock or 'ebb' phase of injury, body glucose (serum glucose concentration X glucose space) is significantly increased but mass flow to peripheral tissue is only slightly altered. During the 'flow' or hypermetabolic phase of injury, mass flow of glucose is markedly increased, related to the extent of injury and directed primarily by increased sympathetic nervous system activity. Increased hepatic gluconeogenesis provides glucose which is converted to three-carbon precursors in the periphery and returns to the liver for reconversion to new glucose, utilising the Cori and alanine cycles.

Insulin response to glucose in hypermetabolic burn patients.

Fifty-four intravenous glucose tolerance tests were performed in 12 normal individuals and 21 thermally injured patients. In the 17 hypermetabolic burn patients studied between the 6th and 16th days postinjury, fasting blood glucose was elevated (111 +/- 7 mg/100 ml, mean +/- SE compared to 85 +/- 3 in controls, P less than 0.001), but the instantaneous proportionality constant for glucose disappearance (k) was similar to that obtained in normal individuals (5.

Alterations in hypothalamic function following thermal injury.

Nine burn patients with a mean burn size of 39% (range, 23-65%) and five normal individuals studied in an environmental chamber selected optimal comfort temperature by regulating a bedside temperature control unit. The normal individuals selected 27.8 degrees C plus or minus 0.

Effect of ambient temperature on heat production and heat loss in burn patients.

Four controls and eight burned patients with thermal injury ranging from 7 to 84% total body surface were studied in an environmental chamber at 25 and 33 degrees C ambient temperature and a constant vapor pressure during two consecutive 24-h periods. Hypermetabolism was present in the burn patients in both ambient temperatures and core and skin temperatures were consistently higher than in the normal men despite increased evaporative water loss. The higher environmental temperature decreased metabolic rate in patients with large thermal injuries in whom the decrement in dry heat loss produced by higher ambient temperature exceeded the increase of wet heat loss.

Catecholamines: mediator of the hypermetabolic response to thermal injury.

Hypermetabolism characterizes the metabolic response to thermal injury and the extent of energy production is positively related to the rate of urinary catecholamine excretion. Alpha and beta adrenergic blockade decreased metabolism from 69.6 +/- 5.