title: Hypertonic saline modulation of intestinal tissue stress and fluid balance.
abstract: Crystalloid-based resuscitation of severely injured trauma patients leads to intestinal edema. A potential mechanism of intestinal edema-induced ileus is a reduction of myosin light chain phosphorylation in intestinal smooth muscle. We sought to determine if the onset of edema initiated a measurable, early mechanotransductive signal and if hypertonic saline (HS) can modulate this early signal by changing intestinal fluid balance. An anesthetized rat model of acute interstitial intestinal edema was used. At laparotomy, the mesenteric lymphatic was cannulated to measure lymph flow and pressure, and a fluid-filled micropipette was placed in the intestinal submucosa to measure interstitial pressure. Rats were randomized into four groups (n=6 per group): sham, mesenteric venous hypertension+80 mL/kg 0.9% isotonic sodium chloride solution (ISCS 80), mesenteric venous hypertension+80 mL/kg 0.9% ISCS+4 mL/kg 7.5% saline (ISCS 80+HS), or 4 mL/kg 7.5% saline (HS alone) to receive the aforementioned intravenous fluid administered over 5 min. Measurements were made 30 min after completion of the preparation. Tissue water, lymph flow, and interstitial pressure were measured. Resultant applied volume induced stress on the smooth muscle (sigmaravi-muscularis) was calculated. Mesenteric venous hypertension and crystalloid resuscitation caused intestinal edema that was prevented by HS. Intestinal edema caused an early increase in intestinal interstitial pressure that was prevented by HS. Hypertonic saline did not augment lymphatic removal of intestinal edema. sigmaravi-muscularis was increased with onset of edema and prevented by HS, paralleling the interstitial pressure data. Intestinal edema causes an early increase in interstitial pressure that is prevented by HS. Prevention of the edema-induced increase in interstitial pressure serves to blunt the mechanotransductive signal of sigmaravi-muscularis.
authors.affiliation: Center for Microvascular and Lymphatic Studies, Department of Surgery, Division of Pediatric Surgery, University of Texas-Houston Medical School, Houston, TX 77030, USA. Charles.S.Cox@uth.tmc.edu
authors.forename: Charles S
authors.initials: CS
authors.lastname: Cox
authors.forename: Ravi
authors.initials: R
authors.lastname: Radhakrishnan
authors.forename: Lindsey
authors.initials: L
authors.lastname: Villarrubia
authors.forename: Hasen
authors.initials: H
authors.lastname: Xue
authors.forename: Karen
authors.initials: K
authors.lastname: Uray
authors.forename: Brijesh S
authors.initials: BS
authors.lastname: Gill
authors.forename: Randolph H
authors.initials: RH
authors.lastname: Stewart
authors.forename: Glen A
authors.initials: GA
authors.lastname: Laine
mesh_terms: D000818:Animals; D004487:Edema / Q000473:pathology; D006973:Hypertension; D007413:Intestinal Mucosa / Q000378:metabolism*; D008297:Male; D008954:Models, Biological; D008962:Models, Theoretical; D009130:Muscle, Smooth / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation; D012492:Salts / Q000494:pharmacology*; D012965:Sodium Chloride / Q000494:pharmacology; D014882:Water-Electrolyte Balance
chemical_list: D012492:Salts; D012965:Sodium Chloride