This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Kles, K.A. Articles by Tappenden, K.A. Search for Related Content PubMed PubMed Citation Articles by Kles, K.A. Articles by Tappenden, K.A. Social Bookmarking                         What's this?

Luminal Nutrients Exacerbate Intestinal Hypoxia in the Hypoperfused Jejunum

Division of Nutritional Sciences, University of Illinois at Urbana-Champaign

M.A. Wallig, PhD, DVM

Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Department of Veterinary Medicine, University of Illinois at Urbana-Champaign

K.A. Tappenden, PhD, RD

Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, tappende{at}uiuc.edu

Background: Provision of enteral nutrients shortly after traumatic injury has become the preferred method of nutrition support provided to patients. However, traumatic shock results in splanchnic hypoperfusion, which may cause persistent intestinal hypoxia. This study tested the hypothesis that delivery of enteral nutrients to the hypoperfused jejunum increases oxidative demand beyond that available, thereby exacerbating intestinal hypoxia. Methods: Wistar-Furth rats (186 ± 4 g; n = 24) were randomized to receive intestinal hypoxia (superior mesenteric artery occlusion) or serve as normoxic controls (sham laparotomy). Within the jejunum of each rat, 4 6-cm loops were randomized to receive luminal perfusions with 1 of 4 substrates: mannitol (an osmotic control); glucose (undergoes active transport via the sodium-glucose co-transporter [SGLT-1] and is metabolized); 3-o-methylglucose (3-o-mg; uses SGLT-1 but is not metabolized); or fructose (does not use SGLT-1 but is metabolized). After in situ perfusions, jejunal tissue was removed for analysis of nutrient transport and barrier function in modified Ussing chambers. Tissue homogenate was used to determine concentration of ATP, lactate, pyruvate, and protein. Also, jejunal tissue was stained with hematoxylin and eosin for qualitative analysis of ischemia and necrosis. Results: Transmural resistance was lower (p < .001) in the hypoxia groups, irrespective of substrate, indicating increased mucosal permeability. When compared with the normoxic controls, glucose transport was impaired (p < .001) in the hypoxic groups; however, glutamine transport was unaffected. The degree of intestinal hypoxia, assessed by jejunal lactate concentration, was higher (p < .001) in the glucose and fructose groups, than the control mannitol and 3-o-mg groups. Conclusions: The observation that 3-o-mg did not differ from the mannitol control indicates that SGLT-1 activation alone does not exacerbate hypoxia. Rather, these results indicate that provision of metabolizable nutrients to the hypoperfused intestine exacerbate hypoxia and potentially lead to intestinal ischemia. Although early enteral nutrition is an important intervention after trauma, care must be taken to ensure intestinal perfusion is adequate to allow for nutrient metabolism and prevent further compromise. (Journal of Parenteral and Enteral Nutrition 25:246-253, 2001)

Journal of Parenteral and Enteral Nutrition, Vol. 25, No. 5, 246-253 (2001)
DOI: 10.1177/0148607101025005246


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				G. Cresci and J. Cue The Patient With Circulatory Shock: To Feed or Not to Feed? Nutr Clin Pract, October 1, 2008; 23(5): 501 - 509. [Abstract] [Full Text] [PDF]

				C. J. Apanavicius, K. L. Powell, B. M. Vester, L. K. Karr-Lilienthal, L. L. Pope, N. D. Fastinger, M. A. Wallig, K. A. Tappenden, and K. S. Swanson Fructan Supplementation and Infection Affect Food Intake, Fever, and Epithelial Sloughing from Salmonella Challenge in Weanling Puppies J. Nutr., August 1, 2007; 137(8): 1923 - 1930. [Abstract] [Full Text] [PDF]

				N. J. Correa-Matos, S. M. Donovan, R. E. Isaacson, H. R. Gaskins, B. A. White, and K. A. Tappenden Fermentable Fiber Reduces Recovery Time and Improves Intestinal Function in Piglets Following Salmonella typhimurium Infection J. Nutr., June 1, 2003; 133(6): 1845 - 1852. [Abstract] [Full Text] [PDF]

				K. A. Kles and K. A. Tappenden Hypoxia differentially regulates nutrient transport in rat jejunum regardless of luminal nutrient present Am J Physiol Gastrointest Liver Physiol, December 1, 2002; 283(6): G1336 - G1342. [Abstract] [Full Text] [PDF]

				D. A. Spain When Is the Seriously III Patient Ready to Be Fed? JPEN J Parenter Enteral Nutr, November 1, 2002; 26(6_suppl): S62 - S68. [Abstract] [PDF]

				J. E. Conour, D. Ganessunker, K. A. Tappenden, S. M. Donovan, and H. R. Gaskins Acidomucin goblet cell expansion induced by parenteral nutrition in the small intestine of piglets Am J Physiol Gastrointest Liver Physiol, November 1, 2002; 283(5): G1185 - G1196. [Abstract] [Full Text] [PDF]