Document Detail


Hypertonic saline modulation of intestinal tissue stress and fluid balance.
MedLine Citation:
PMID:  18414233     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Charles S Cox; Ravi Radhakrishnan; Lindsey Villarrubia; Hasen Xue; Karen Uray; Brijesh S Gill; Randolph H Stewart; Glen A Laine
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  29     ISSN:  1073-2322     ISO Abbreviation:  Shock     Publication Date:  2008 May 
Date Detail:
Created Date:  2008-04-16     Completed Date:  2008-06-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  598-602     Citation Subset:  IM    
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
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MeSH Terms
Descriptor/Qualifier:
Animals
Edema / pathology
Hypertension
Intestines / metabolism*
Male
Models, Biological
Models, Theoretical
Muscle, Smooth / pathology
Myocytes, Smooth Muscle / metabolism
Rats
Rats, Sprague-Dawley
Resuscitation
Salts / pharmacology*
Sodium Chloride / pharmacology
Water-Electrolyte Balance
Grant Support
ID/Acronym/Agency:
5K08 GM00675/GM/NIGMS NIH HHS; CCU-620069//PHS HHS; P30 DK56338/DK/NIDDK NIH HHS; P50 GM38529/GM/NIGMS NIH HHS; R01 HL36115/HL/NHLBI NIH HHS; T32 GM08792/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Salts; 7647-14-5/Sodium Chloride

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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