Document Detail

Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability.
MedLine Citation:
PMID:  2188748     Owner:  NLM     Status:  MEDLINE    
Resistance to endotoxin in essential fatty acid-deficient (EFAD) rats is associated with reduced synthesis of certain arachidonic acid metabolites. It was hypothesized that EFAD rats would manifest decreased vascular permeability changes during endotoxemia as a consequence of reduced arachidonic acid metabolism. To test this hypothesis, changes in hematocrit (HCT) and mesenteric localization rate of technetium-labeled human serum albumin (99mTc-HSA) and red blood cells (99mTc-RBC) were assessed in EFAD and normal rats using gamma-camera imaging. Thirty minutes after Salmonella enteritidis endotoxin, EFAD rats exhibited less hemoconcentration as determined by % HCT than normal rats (47 +/- 2% vs. 54 +/- 1% respectively, P less than 0.01). Endotoxin caused a less severe change in permeability index in the splanchnic region in EFAD rats than in normal rats (1.2 +/- 0.6 x 10(-3)min-1 vs. 4.9 +/- 1.7 x 10(-3)min-1 respectively, P less than 0.05). In contrast to 99mTc-HSA, mesenteric localization of 99mTc-RBC was not changed by endotoxin in control or EFAD rats. Supplementation with ethyl-arachidonic acid did not enhance susceptibility of EFAD rats to endotoxin-induced splanchnic permeability to 99mTc-HSA. Leukotrienes have been implicated as mediators of increased vascular permeability in endotoxin shock. Since LTC3 formation has been reported to be increased in EFA deficiency, we hypothesized that LTC3 may be less potent than LTC4. Thus the effect of LTC3 on mean arterial pressure and permeability was compared to LTC4 in normal rats. LTC3-induced increases in peak mean arterial pressure were less than LTC4 at 10 micrograms/kg (39 +/- 5 mm Hg vs. 58 +/- 4 mm Hg respectively, P less than 0.05) and at 20 micrograms/kg (56 +/- 4 mm Hg vs. 75 +/- 2 mm Hg respectively, P less than 0.05). LY171883 (30 mg/kg), an LTD4/E4 receptor antagonist, attenuated the pressor effect of LTC4, LTD4, and LTC3. Infusion of LTC4 (4 micrograms/kg/min) in normal rats induced a rise in HCT from 44 +/- 1% to 51 +/- 1% (P less than 0.01), which was greater (P less than 0.05) than the rise induced by LTC3 (47 +/- 1% to 49 +/- 1%). The results showing that EFAD rats are resistant to endotoxin-induced increases in HCT and vascular permeability raise the possibility that this may, in part, be a result of preferential LTC3 production that is less potent than LTC4.
E J Li; J A Cook; K M Spicer; W C Wise; J Rokach; P V Halushka
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulatory shock     Volume:  31     ISSN:  0092-6213     ISO Abbreviation:  Circ. Shock     Publication Date:  1990 Jun 
Date Detail:
Created Date:  1990-06-29     Completed Date:  1990-06-29     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0414112     Medline TA:  Circ Shock     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  159-70     Citation Subset:  IM    
Department of Physiology, Medical University of South Carolina, Charleston 29425.
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MeSH Terms
Blood Pressure / drug effects
Capillary Permeability*
Fatty Acids, Essential / deficiency*
SRS-A / analogs & derivatives,  pharmacology
Salmonella enteritidis
Serum Albumin
Shock, Septic / chemically induced,  physiopathology*
Grant Support
Reg. No./Substance:
0/Endotoxins; 0/Fatty Acids, Essential; 0/SRS-A; 0/Serum Albumin; 7440-26-8/Technetium; 77209-77-9/leukotriene C-3

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