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Severe Chloride Deficiency in the Neonate: The Canine Puppy as an Animal Model
Journal article   Open access   Peer reviewed

Severe Chloride Deficiency in the Neonate: The Canine Puppy as an Animal Model

Christian C Felder, Jean E Robillard, Shane Roy and Pedro A Jose
Pediatric research, Vol.21(5), pp.497-501
05/1987
DOI: 10.1203/00006450-198705000-00015
PMID: 3588090
url
https://doi.org/10.1203/00006450-198705000-00015View
Published (Version of record) Open Access

Abstract

Studies were designed to develop an animal model for the syndrome of hypochloremic, hypokalemic metabolic alkalosis (HMA), and failure to thrive in infants due to intake of chloride-deficient formula. Littermate canine puppies, 2 wk old, were fed soy formula containing normal chloride, 20 mEq/liter (NC, n = 5), or low chloride, 1 mEq/liter (LC, n = 5) for 4 wk, first by gavage and ad libitum thereafter. After 1 wk of LC formula, HMA developed in LC puppies although both NC and LC puppies had similar fluid and caloric intake and gain in weight and forelimb length. Two wk of LC formula also resulted in a 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. Plasma renin activity decreased with age in NC but remained elevated in LC. In a separate group of puppies (n = 6) with HMA, chloride supplementation of LC formula as NaCl to NC levels corrected HMA despite continued citrate intake. We conclude that the canine puppy is an appropriate model to study HMA due to decreased chloride intake. Low chloride intake independent of citrate caused the HMA.

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