Abstract

Extract: The influence of disaccharides on the development of systemic acidosis in premature infants was studied by observing the changes that occurred in the blood after oral administration of carbohydrates. Lactose produced a small rise in levels of reducing sugar in blood, a stepwise increase of lactate concentrations, and a simultaneous drop in blood pH and CO2 in serum. There were no acid-base alterations, and there was a greater increment in reducing sugars in blood in full-term patients with intrauterine malnutrition (IUM) and in premature infants after month 2 of life. In premature infants the drop in pH induced by lactose was significant during the first 15 min after the oral load and reached the lowest level (mean drop 0.09 pH unit) within 30–45 min with gradual return to the basal point at 120 min. The maximal decrease in bicarbonate concentrations (mean drop 2.63 mEq/liter) occurred at 60–90 min after lactose feeding and was associated with a decrease in chloride concentration in serum (mean drop 7.8 mEq/liter) and an increased sodium-to-chloride ratio. The increase in levels of lactate in blood did not account for the fall in levels of chloride and could only relate one-ninth of the anion substitution that occurred. In contrast, an equimolar load of mannitol induced none of the above mentioned changes. Stool composition after lactose loading did not vary in infants given oral loads of carbohydrates. When the maximal functional capacity was exceeded, however, diarrhea was induced, the pH of the stool dropped to a low of 4.50, and carbohydrates, lactate, and electrolytes were excreted in increased amounts in the feces; simultaneously severe metabolic acidosis ensued. The development of metabolic acidosis after oral loads of lactose was modified neither by neomycin treatment nor by substrate priming. There was an improvement in the response, however, as the infants grew older; those infants who received lactose during day 1 of extrauterine life were the infants who had the most striking decreases in blood pH values (mean 7.27) and bicarbonate concentrations in serum (mean 17.6 mEq/liter). An oral load of sucrose also produced a small rise in levels of reducing sugars in blood and induced metabolic acidosis, although the response was less intense than that obtained after lactose administration. There was no impairment in monosaccharide metabolism; the absorption of glucose, galactose, and fructose was normal; and the blood pH values remained stable throughout. All carbohydrates induced lactic acidemia similar to that produced by lactose.

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