Effects of intravenous glucose loading on oxygen consumption, carbon dioxide production, and resting energy expenditure in infants with bronchopulmonary dysplasia.
To determine the effects of intravenous glucose loading on basal oxygen consumption, resting energy expenditure, and basal carbon dioxide production in infants with bronchopulmonary dysplasia who were still oxygen dependent, we administered intravenous glucose loads of 4 and 12 mg/kg-1/min-1 on 2 consecutive days, under identical experimental conditions, to six infants with bronchopulmonary dysplasia and six healthy control subjects. Infants were not fed for 9 hours before and during the 4- to 6-hour study periods; the intravenous glucose infusion, along with an amino acid mixture (2 gm.kg-1.24 hr-1), was started at the beginning of the fasting period. Oxygen consumption and carbon dioxide production and resting energy expenditure were measured by a flow-through indirect calorimetry technique under basal conditions. Infants with oxygen-dependent bronchopulmonary dysplasia had significantly higher basal oxygen consumption and resting energy expenditure than did control infants and significantly higher basal carbon dioxide production during the high glucose infusion. With glucose loading, infants with bronchopulmonary dysplasia had a significant rise in basal oxygen consumption (7.91 +/- 0.91 ml.kg-1.min-1 to 9.65 +/- 1.35 ml.kg-1.min-1, p less than 0.05), basal carbon dioxide production (5.93 +/- 0.72 ml.kg-1.min-1 to 7.10 +/- 1.04 ml.kg-1.min-1), and resting energy expenditure (53.8 +/- 5.75 kcal.kg-1.24 hr-1 to 65.3 +/- 7.0 kcal.kg-1.24 hr-1, all p values less than 0.05). Control infants had no significant changes with intravenous glucose loading. We conclude that intravenous glucose loading in infants with bronchopulmonary dysplasia resulted in a net increase in resting energy expenditure, which should be taken into account in assessing their energy intake during nutritional management. The risk of pulmonary stress caused by an increase in basal oxygen consumption and carbon dioxide production resulting from glucose load should also be considered.
Yunis
K A
KA
Brown University Program in Medicine, Women and Infants' Hospital of Rhode Island, Providence 02905-2499.
Oh
W
W
D001997:Bronchopulmonary Dysplasia / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000096:biosynthesis; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D010101:Oxygen Consumption / Q000187:drug effects*
D002245:Carbon Dioxide; D005947:Glucose