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Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F13%3A43907279%21RIV14-MSM-11120___
rdf:type
skos:Concept n17:Vysledek
dcterms:description
Septic shock has a high mortality rate, partially related to myocardial dysfunction. Polyunsaturated fatty acids (omega-3 PUFAs) possess anti-inflammatory and antioxidant properties, but whether omega-3 PUFAs exert beneficial effects on myocardial function is unknown. We investigated, in a rat model of endotoxic shock, the effects of omega-3 PUFAs pretreatment on cardiac hemodynamics, function, and oxidative stress as well as intestinal barrier. Endotoxic shock was induced by lipopolysaccharide (LPS; 20 mg/kg IP) administered to rats pretreated or not with omega-3 PUFAs (Omegaven; 0.5 g/kg IP, 90 min before injection of LPS). Two or 5 h after LPS, left ventricular function and arterial pressure were measured, followed by assessment left ventricular total glutathione as well as tumor necrosis factor alpha expression, occuldin expression, and proteasome activities. LPS reduced mean arterial blood pressure to the same extent 2 and 5 h after its administration, but cardiac output was more markedly decreased after 5 h. Omega-3 PUFAs pretreatment did not significantly modify the effect of LPS on mean arterial pressure and total peripheral resistance, but prevented the decrease in cardiac output 2 h after LPS. LPS increased oxidized glutathione after 2 h, and this increase was significantly attenuated by omega-3 PUFAs. Simultaneously, omega-3 PUFAs increased myocardial hemeoxygenase-1 (HO-1) mRNA expression. Finally, omega-3 PUFAs prevented the reduction of intestinal occludin expression. Omega-3 PUFAs pre-treatment improves myocardial dysfunction during endotoxemia and increases myocardial HO-1 expression. Moreover, the preservation of the intestinal occludin induced by omega-3 PUFAs precedes myocardial protection, suggesting the involvement of the intestinal barrier in the myocardial improvement observed with omega-3 PUFAs parenteral supplementation. Septic shock has a high mortality rate, partially related to myocardial dysfunction. Polyunsaturated fatty acids (omega-3 PUFAs) possess anti-inflammatory and antioxidant properties, but whether omega-3 PUFAs exert beneficial effects on myocardial function is unknown. We investigated, in a rat model of endotoxic shock, the effects of omega-3 PUFAs pretreatment on cardiac hemodynamics, function, and oxidative stress as well as intestinal barrier. Endotoxic shock was induced by lipopolysaccharide (LPS; 20 mg/kg IP) administered to rats pretreated or not with omega-3 PUFAs (Omegaven; 0.5 g/kg IP, 90 min before injection of LPS). Two or 5 h after LPS, left ventricular function and arterial pressure were measured, followed by assessment left ventricular total glutathione as well as tumor necrosis factor alpha expression, occuldin expression, and proteasome activities. LPS reduced mean arterial blood pressure to the same extent 2 and 5 h after its administration, but cardiac output was more markedly decreased after 5 h. Omega-3 PUFAs pretreatment did not significantly modify the effect of LPS on mean arterial pressure and total peripheral resistance, but prevented the decrease in cardiac output 2 h after LPS. LPS increased oxidized glutathione after 2 h, and this increase was significantly attenuated by omega-3 PUFAs. Simultaneously, omega-3 PUFAs increased myocardial hemeoxygenase-1 (HO-1) mRNA expression. Finally, omega-3 PUFAs prevented the reduction of intestinal occludin expression. Omega-3 PUFAs pre-treatment improves myocardial dysfunction during endotoxemia and increases myocardial HO-1 expression. Moreover, the preservation of the intestinal occludin induced by omega-3 PUFAs precedes myocardial protection, suggesting the involvement of the intestinal barrier in the myocardial improvement observed with omega-3 PUFAs parenteral supplementation.
dcterms:title
Omega-3 Polyunsaturated Fatty Acids Delay the Progression of Endotoxic Shock-Induced Myocardial Dysfunction Omega-3 Polyunsaturated Fatty Acids Delay the Progression of Endotoxic Shock-Induced Myocardial Dysfunction
skos:prefLabel
Omega-3 Polyunsaturated Fatty Acids Delay the Progression of Endotoxic Shock-Induced Myocardial Dysfunction Omega-3 Polyunsaturated Fatty Acids Delay the Progression of Endotoxic Shock-Induced Myocardial Dysfunction
skos:notation
RIV/00216208:11120/13:43907279!RIV14-MSM-11120___
n17:predkladatel
n18:orjk%3A11120
n4:aktivita
n15:S
n4:aktivity
S
n4:cisloPeriodika
4
n4:dodaniDat
n9:2014
n4:domaciTvurceVysledku
n5:7627068
n4:druhVysledku
n16:J
n4:duvernostUdaju
n6:S
n4:entitaPredkladatele
n13:predkladatel
n4:idSjednocenehoVysledku
93619
n4:idVysledku
RIV/00216208:11120/13:43907279
n4:jazykVysledku
n11:eng
n4:klicovaSlova
TNF; omega-3; myocardial dysfunction; intestinal permeability; hemeoxygenase-1; endotoxic shock; cytokine
n4:klicoveSlovo
n7:hemeoxygenase-1 n7:omega-3 n7:TNF n7:endotoxic%20shock n7:myocardial%20dysfunction n7:intestinal%20permeability n7:cytokine
n4:kodStatuVydavatele
US - Spojené státy americké
n4:kontrolniKodProRIV
[ABBD82B56660]
n4:nazevZdroje
Inflammation
n4:obor
n10:FB
n4:pocetDomacichTvurcuVysledku
1
n4:pocetTvurcuVysledku
9
n4:rokUplatneniVysledku
n9:2013
n4:svazekPeriodika
36
n4:tvurceVysledku
Kušíková, Eva
n4:wos
000321641300018
s:issn
0360-3997
s:numberOfPages
8
n14:organizacniJednotka
11120