Linked Life Data

8985066

Source:http://linkedlifedata.com/resource/pubmed/id/8985066

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-1-23
pubmed:abstractText
This study was undertaken to evaluate the role of nitric oxide (NO) in the sepsis-induced disruption of intracellular calcium homeostasis and membrane dynamics. Anticoagulated whole blood was obtained from 10 healthy volunteers. Equal aliquots were incubated with saline (control), 2 microg/mL Escherichia coli endotoxin (lipopolysaccharide), 8 microg/mL NO inhibitor, N-monomethyl arginine (NMA), and endotoxin plus NO inhibitor (lipopolysaccharide/NMA). Erythrocytes were harvested, washed, and loaded with the calcium chelator, FURA-2AM, and the fluorescent membrane probe TMA-DPH. Cells were evaluated for both intracellular calcium concentration and membrane viscosity (anisotropy) by fluorescent spectrophotometry. Endotoxin induced a significant increase in both intracellular calcium concentration and anisotropy. NMA had no intrinsic affect on either of these cellular characteristics. NMA was, however, effective in preventing the endotoxin-induced changes. These results suggest that NO may play a role in the disruption of intracellular calcium homeostasis and erythrocyte membrane deformability noted in sepsis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0003-1348
pubmed:author
pubmed:issnType
Print
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
20-3
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Nitric oxide synthase inhibition negates septic-induced alterations in cytoplasmic calcium homeostasis and membrane dynamics.
pubmed:affiliation
University of Florida Health Science Center Jacksonville, 32209, USA.
pubmed:publicationType
Journal Article