Linked Life Data

11019959

Source:http://linkedlifedata.com/resource/pubmed/id/11019959

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-1-8
pubmed:abstractText
The influence of adenosine infusion (40 microg/kg/min for 4 h) on inflammatory and hemostatic parameters was investigated in healthy males without (n = 10) or with (n = 11) intravenous endotoxin injection (4 ng/kg). Without endotoxin, adenosine elevated circulating leukocytes and circulating platelet-leukocyte aggregates. Endotoxin activated platelets and leukocytes in vivo. Platelet activation was seen as slightly increased platelet P-selectin expression, decreased platelet counts, and elevated plasma soluble P-selectin (from 39.6 +/- 3.4 to 68.9 +/- 6.6 ng/ml, P<0.01). Leukocyte activation was evidenced by increased CD1 lb expression (from MFI of 0.54 +/- 0.02 to 2.21 +/- 0.17; P<0.01) and plasma elastase levels (from 25.3 +/- 2.5 to 169.3 +/- 22.5 ng/ml: P <0.01). Endotoxin also enhanced platelet and leukocyte responsiveness to in vitro stimulation. Endotoxin induced von Willebrand factor secretion (from 92 +/- 8 units to 265 +/- 19 units at 4 h; P <0.001) and enhanced thrombin generation in vivo. Endotoxin induced leukocytosis and thus increased circulating platelet-leukocyte, mainly platelet-neutrophil, aggregates. Adenosine caused slight attenuation of platelet reactivity to agonist stimulation, enhanced the endotoxin-induced leukocytosis, and detained more platelet-leukocyte aggregates in circulation, but did not attenuate endotoxin-induced neutrophil elastase secretion, von Willebrand factor secretion, or thrombin generation. Thus, endotoxemia induces multi-cellular activation in vivo. Adenosine inhibits leukocyte adhesion and extravasation, and mildly attenuates platelet responsiveness and soluble P-selectin release. Adenosine has the potential of becoming a therapeutic antiinflammatory drug, but an optimal treatment strategy needs to be developed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0340-6245
pubmed:author
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
381-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11019959-Adenosine, pubmed-meshheading:11019959-Adult, pubmed-meshheading:11019959-Cell Adhesion, pubmed-meshheading:11019959-Cross-Over Studies, pubmed-meshheading:11019959-Double-Blind Method, pubmed-meshheading:11019959-Endotoxins, pubmed-meshheading:11019959-Hematologic Tests, pubmed-meshheading:11019959-Hemodynamics, pubmed-meshheading:11019959-Humans, pubmed-meshheading:11019959-Inflammation, pubmed-meshheading:11019959-Infusions, Intravenous, pubmed-meshheading:11019959-Leukocytes, pubmed-meshheading:11019959-Macrophage-1 Antigen, pubmed-meshheading:11019959-Male, pubmed-meshheading:11019959-P-Selectin, pubmed-meshheading:11019959-Peptide Fragments, pubmed-meshheading:11019959-Placebos, pubmed-meshheading:11019959-Platelet Activation, pubmed-meshheading:11019959-Prothrombin, pubmed-meshheading:11019959-von Willebrand Factor
pubmed:year
2000
pubmed:articleTitle
Multi-cellular activation in vivo by endotoxin in humans--limited protection by adenosine infusion.
pubmed:affiliation
Department of Medicine, Karolinska Hospital, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Clinical Trial, Comparative Study, Randomized Controlled Trial, Research Support, Non-U.S. Gov't