title: Hypertonic saline resuscitation prevents hydrostatically induced intestinal edema and ileus.
abstract: OBJECTIVE
  We have shown that acute edema induced by mesenteric venous hypertension (MV-HTN) impairs intestinal transit and reduces the standardized engineering measures of intestinal stiffness (elastic modulus) and residual stress (opening angle). We hypothesized that hypertonic saline (7.5%) would reverse these detrimental effects of acute edema.
  
  
  METHODS
  Laboratory study.
  
  
  METHODS
  University laboratory.
  
  
  METHODS
  Male Sprague Dawley rats (270-330 g).
  
  
  METHODS
  Rats were randomized to five groups: sham, MV-HTN alone, MV-HTN with 4 mL/kg normal saline resuscitation (equal volume), MV-HTN with 33 mL/kg normal saline resuscitation (equal salt), and MV-HTN with 4 mL/kg hypertonic saline. Intestinal edema was measured by wet to dry tissue weight ratio. A duodenal catheter was placed and, 30 mins before death, fluorescein isothiocyanate Dextran was injected. At death, dye concentrations were measured to determine intestinal transit. Segments of distal ileum were hung to a fixed point in a tissue bath and to a force displacement transducer and stretched in increments of 1 mm; we recorded the new length and the corresponding force from the force displacement transducer to determine elastic modulus. Next, two transverse cuts were made yielding a 1- to 2-mm thick ring-shaped segment of tissue which was then cut radially to open the ring. Then the opening angle was measured.
  
  
  RESULTS
  MV-HTN, MV-HTN with 4 mL/kg normal saline, and MV-HTN with 33 mL/kg normal saline caused a significant increase in tissue edema and a significant decrease in intestinal transit, stiffness, and residual stress compared with sham. Hypertonic saline significantly lessened the effect of edema on intestinal transit and prevented the changes in stiffness and residual stress.
  
  
  CONCLUSIONS
  Hypertonic saline prevented intestinal tissue edema. In addition, hypertonic saline improved intestinal transit, possibly through more efficient transmission of muscle force through stiffer intestinal tissue.
authors.affiliation: Department of Surgery, University of Texas-Houston Medical School, Houston, TX, USA.
authors.forename: Ravi S
authors.initials: RS
authors.lastname: Radhakrishnan
authors.forename: Hasen
authors.initials: H
authors.lastname: Xue
authors.forename: Stacey D
authors.initials: SD
authors.lastname: Moore-Olufemi
authors.forename: Norman W
authors.initials: NW
authors.lastname: Weisbrodt
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Moore
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Allen
authors.forename: Glen A
authors.initials: GA
authors.lastname: Laine
authors.forename: Charles S
authors.initials: CS
authors.lastname: Cox
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004487:Edema / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D045823:Ileus / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D009994:Osmolar Concentration; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation / Q000379:methods*; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage / Q000627:therapeutic use*; D012964:Sodium / Q000097:blood; D014690:Venous Pressure
chemical_list: D012462:Saline Solution, Hypertonic; D012964:Sodium