Abstract
Gastrointestinal stasis, bacterial overgrowth and accumulation of toxic bile acids may be etiologically related to total parenteral nutrition (TPN)-associated cholestasis. New Zealand White rabbits were studied to investigate interrelations between these factors. TPN-infused animals received 150 kcal and 5 gm protein/kg/d. Pair-fed animals were fed rabbit chow to supply 5 gm protein/kg/d (PF). Free-fed animals ate >5 gm protein/kg/d (FF). Gastrointestinal transit time, as assessed by a solid marker technique, was <48h in 95% of fed animals and >72 h in 100% of TPN animals. Colons of TPN animals contained bilious liquid rather than semi-solid feces. There was no bacterial overgrowth in duodenal contents in any animal; gall bladder bile was sterile. Although the Mole. % total primary bile acids (BA) and total secondary BA were equivalent in gall bladder bile in the 3 groups, the Mole % glycolithocholic acid (GLCA) was significantly increased (p<.001) in TPN animals (4.28 Mol%) compared to PF (1.68 Mol%) and FF (1.35 Mol%). Serum total primary BA and gamma glutamyl transpeptidase concentrations were higher in TPN animals (p<.02). In this rabbit model TPN led to decreased gastrointestinal motility, increased relative biliary concentration of the toxic monohydroxy bils acid GLCA and increased serum markers of cholestasis. This animal model, which exhibits changes consistent with human TPN-associated cholestasis, should facilitate experimental studies of the etiology of this syndrome.
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Gleqhom, E., Merritt, R., Henton, D. et al. 653 A RABBIT MODEL FOR THE PATHOPHYSIOLOGY OF TOTAL PARENTERAL NUTRITION-ASSOCIATED CHOLESTASIS. Pediatr Res 19, 219 (1985). https://doi.org/10.1203/00006450-198504000-00683
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DOI: https://doi.org/10.1203/00006450-198504000-00683