title: Ischemia/reperfusion-induced disruption of rat small intestine transit is reversed by total enteral nutrition.
abstract: OBJECTIVE
  A reduced blood flow to the gut is a consistent event after traumatic shock. Enteral nutrition support has been shown to reduce the septic morbidity after major trauma. We evaluated the effects of a transient ischemia followed by reperfusion (I/R) and an enteral nutrition support regimen on the motility of the small intestine of the rat.
  
  
  METHODS
  A catheter was placed in the upper duodenum and the small intestine was then made ischemic by clamping the superior mesenteric artery for 45 min; the arteries of sham rats were isolated but not clamped. Intestinal transit was evaluated by measuring the amount of fluorescein isothiocyanate-dextran (12 000 MW) in each of 10 intestinal sections at 30 min after injection through the duodenal catheter. The mean geometric center of marker distribution (MGC) was calculated for each group and compared. In a second study, I/R was followed by infusion of saline or a complete nutrient solution overnight, and transit was determined.
  
  
  RESULTS
  Intestinal transit (as the MGC) of I/R rats at 24 h after the beginning of reperfusion (3.5 +/- 0.2) and 48 h after the beginning of reperfusion (4.5 +/- 1.1) was significantly lower than that in the respective sham controls (5.1 +/- 0.3 and 5.9 +/- 0.5). The MGC for rats receiving a nutrient solution overnight during the reperfusion phase (6.0 +/- 1.1) was significantly increased compared with the MGC of 4.8 +/- 0.3 for rats receiving saline during the same period.
  
  
  CONCLUSIONS
  These results demonstrate a long-term deleterious effect of a non-lethal ischemia on intestinal transit and may be one explanation for many of the sequelae occurring after ischemia. In addition, these results demonstrate that a nutrient infusion will prevent the delayed transit. This may provide a partial explanation for the beneficial effects of total enteral nutrition in the clinical situation of posttraumatic injury.
authors.affiliation: Department of Integrative Biology, University of Texas Medical School at Houston, Houston, Texas, USA. bgrossie@twu.edu
authors.forename: V B
authors.initials: VB
authors.lastname: Grossie
authors.forename: N W
authors.initials: NW
authors.lastname: Weisbrodt
authors.forename: F A
authors.initials: FA
authors.lastname: Moore
authors.forename: F
authors.initials: F
authors.lastname: Moody
mesh_terms: D000818:Animals; D003911:Dextrans; D004195:Disease Models, Animal; D004750:Enteral Nutrition; D016650:Fluorescein-5-isothiocyanate / Q000031:analogs & derivatives; D005769:Gastrointestinal Motility; D005772:Gastrointestinal Transit; D007421:Intestine, Small / Q000503:physiopathology*; D007511:Ischemia / Q000503:physiopathology / Q000628:therapy*; D007700:Kinetics; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000503:physiopathology / Q000628:therapy*
chemical_list: D003911:Dextrans; C015219:fluorescein isothiocyanate dextran; D016650:Fluorescein-5-isothiocyanate