Linked Life Data

12923500

Source:http://linkedlifedata.com/resource/pubmed/id/12923500

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-8-18
pubmed:abstractText
Because gut-derived factors carried in mesenteric lymph are implicated in multiple organ dysfunction syndrome and have been shown to injure endothelial cells, we investigated several cellular pathways by which this process could occur. To accomplish this, mesenteric lymph (5%, v/v) collected at 1 to 3 h postshock from male rats undergoing trauma (5-cm laparotomy) and hemorrhagic shock (90 min of mean arterial pressure [MAP] of 30 mmHg; T/HS) was tested for endothelial cell cytotoxicity on human umbilical vein endothelial cells (HUVECs). Over 30 pharmacologic agents that had been reported to inhibit endothelial cell death were tested for their ability to prevent T/HS lymph-induced HUVEC cell death. These included agents documented to protect against oxidant-mediated, calcium-mediated, and arachidonic acid pathway-mediated endothelial cell injury and death. These pharmacologic inhibitors were preincubated with HUVECs for 1 h or were added to the HUVECs simultaneously with lymph, and were then incubated for 18 h. Controls were lymph alone, inhibitor alone, or medium alone. Mitochondrial tetrazolium (MTT) and LDH release assays were used to determine cell viability. The inhibitors that significantly protected HUVECs from the cytotoxicity of T/HS lymph (P < 0.001) included the antioxidant combination of vitamins C and E and the antioxidant-lipooxygenase inhibitor nordihydroguaretic acid (NDGA). These agents were equally effective when added simultaneously with lymph or preincubated with the HUVECs, suggesting an extracellular or membrane-bound process. In summary, the inhibitors that provided protection from toxic lymph appear to work at the membrane and are involved in limiting membrane peroxidation. Based on this study, it appears that an oxidant pathway is involved in T/HS lymph-induced endothelial cell injury and death.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1073-2322
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
269-73
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12923500-Animals, pubmed-meshheading:12923500-Antioxidants, pubmed-meshheading:12923500-Cell Survival, pubmed-meshheading:12923500-Cells, Cultured, pubmed-meshheading:12923500-Coloring Agents, pubmed-meshheading:12923500-Endothelial Cells, pubmed-meshheading:12923500-Humans, pubmed-meshheading:12923500-L-Lactate Dehydrogenase, pubmed-meshheading:12923500-Lipoxygenase, pubmed-meshheading:12923500-Male, pubmed-meshheading:12923500-Mesentery, pubmed-meshheading:12923500-Nordihydroguaiaretic Acid, pubmed-meshheading:12923500-Oxidants, pubmed-meshheading:12923500-Rats, pubmed-meshheading:12923500-Rats, Sprague-Dawley, pubmed-meshheading:12923500-Shock, pubmed-meshheading:12923500-Tetrazolium Salts, pubmed-meshheading:12923500-Thiazoles, pubmed-meshheading:12923500-Time Factors, pubmed-meshheading:12923500-Umbilical Veins
pubmed:year
2003
pubmed:articleTitle
The role of oxidant-mediated pathways in the cytotoxicity of endothelial cells exposed to mesenteric lymph from rats subjected to trauma-hemorrhagic shock.
pubmed:affiliation
Department of Surgery, New Jersey Medical School, Newark, NJ 07101, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.