ABSTRACT. Studies were designed to develop an animal depletion is responsible for the development of metabolic alkamodel for the syndrome of hypochloremic, hypokalemic losis and resultant electrolyte imbalances (9-1 1). Either citrate metabolic alkalosis (HMA), and failure to thrive in infants alone or in combination with other counter anions used to due to intake of chloride-deficient formula. Littermate replace chloride in soy formulas has also been implicated in the canine puppies, 2 wk old, were fed soy formula containing development of HMA (12, 14). normal chloride, 20 mEq/liter (NC, n = S), or low chloride, Essential to the further study of CDS in human infants is a 1 mEq/liter (LC, n = 5) for 4 wk, first by gavage and ad neonatal animal model that demonstrates the biochemical and libitum thereafter. After 1 wk of LC formula, HMA de-clinical abnormalities characteristic of the disorder in infants. veloped in LC puppies although both NC and LC puppies Therefore, the present study was primarily designed to develop had similar fluid and caloric intake and gain in weight and a neonatal animal model of HMA. In addition, the role of forelimb length. Two wk of LC formula also resulted in a chloride ion in the pathogenesis of HMA was evaluated. higher serum creatinine and calcium but lower phosphate level in LC than NC puppies. After 4 wk of LC, weight and forelimb length were much less in LC than NC puppies.
METHODSPlasma renin activity decreased with age in NC but re-~1 1 experiments were carried out on littermate mongrel canine mained elevated in LC. In a separate group of puppies (n puppies randomly assigned to one of two formulas (Table 1) = 6, with HMA, LC prepared under the direction of the Infant Formula Council to as NaC1 NC levels HMA despite meet the dietary requirements of puppies (15). NC contained 20 citrate intake. We conclude that the canine PUPPY is an mEq/liter chloride and the LC contained 1 mEq/liter chloride. appropriate model to study HMA due to decreased chloride ~0 t h the LC and the NC formulas contained 20 mEq/liter of intake. Low chloride intake independent of citrate caused sodium with citrate added as the counter ion in the LC formula. the HMA. (Pediatr Res 21: 497-501, 1986) The formula containing 1 kcal/ml was fed to the puppies commencing 2 wk following birth. Formula was fed by gavage Abbreviations every 6 h until the puppies were able to feed themselves, which LC, low chloride occurred at about 6 wk of age. At 6 wk of age the animals were NC, normal chloride fed every 8 h. Intake was monitored by measuring the amount CDS, chloride deficiency syndrome of formula given and the amount of formula refused or regurgi-HMA, hypochloremic metabolic alkalosis tated with each feeding. Formula was given to the puppies to PRA, plasma renin activity assure caloric intake of about 160 to 225 kcallkg per day.BUN, blood urea nitrogen Two litters of puppies were studied. The first litter (group I)Cr, creatinine had 10 puppies; five puppies were randomized to the LC group and five to the NC group....