Format

Send to

Choose Destination
See comment in PubMed Commons below
JPEN J Parenter Enteral Nutr. 1998 Nov-Dec;22(6):387-92.

Enterocyte nutrient transport is preserved in a rabbit model of acute intestinal ischemia.

Author information

1
Department of Surgery and Pathology, University of Rochester Medical Center, New York 14642-8410, USA.

Abstract

BACKGROUND:

The use of enteral nutrition in patients with nonocclusive splanchnic hypoperfusion is controversial. This study aims to quantitate enterocyte nutrient transport and correlate function with morphology during intestinal ischemia.

METHODS:

New Zealand White rabbits were randomized to control (celiotomy only) 60-minute infrarenal aortic clamp (IRC) or 60-minute supraceliac aortic clamp (SCC). Small intestinal brush border membrane vesicles (BBMVs) were prepared by magnesium precipitation and serial differential centrifugation. Sodium-dependent uptake of glucose, glutamine, alanine, leucine, and arginine into BBMVs was quantitated by rapid mixing and filtration. Histologic examination of the intestine was performed by a pathologist blinded to groups. Data are reported as mean values+/-SEM, with significance determined by analysis of variance at p < .05.

RESULTS:

Villus heights in the IRC and SCC groups were 20% and 48% less than control, respectively. SCC histology was characterized by extensive epithelial denudation and necrosis, whereas IRC had mild focal villus edema only. Sodium-dependent glucose and leucine transport each exhibited nonsignificant increases of 20% to 25% in the IRC group and 30% to 55% in the SCC group. No changes were noted in sodium-dependent glutamine, alanine, and arginine uptake or sodium-independent transport.

CONCLUSIONS:

Enteral nutrient transport does not correlate with mucosal architecture, is maintained during splanchnic hypoperfusion states, and likely occurs via intact crypt cells.

PMID:
9829613
DOI:
10.1177/0148607198022006387
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Atypon
    Loading ...
    Support Center