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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2 Pt 2
|
pubmed:dateCreated |
1993-4-6
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pubmed:abstractText |
The aim of this study was to determine whether immunoneutralization of the common beta-subunit of the neutrophil CD11/CD18 glycoprotein adherence complex with monoclonal antibody IB4 (mAb IB4) or neutrophil depletion with a specific canine polyclonal antineutrophil serum (ANS) would reduce the extent of no-reflow in postischemic skeletal muscle. Microvascular patency was assessed by infusion of india ink contrast media and quantified by counting ink-containing microvessels < 15 microns diameter in histological sections obtained from isolated canine gracilis muscles subjected to 4.5 h of continuous perfusion (nonischemic control), 4 h of ischemia and 30 min of reperfusion [ischemia/reperfusion (I/R)] alone, I/R plus ANS, and I/R plus mAb IB4. I/R was associated with a marked reduction in microvascular patency compared with nonischemic controls (0.9 +/- 0.1 vs. 2.3 +/- 0.1 ink-containing microvessels per muscle fiber, respectively). Neutrophil depletion or prevention of neutrophil adherence attenuated the I/R-induced reduction in the number of ink-containing capillaries (1.6 +/- 0.1 and 2.2 +/- 0.2 ink-containing microvessels per muscle fiber, respectively). These data indicate that neutrophils play an important role in the genesis of no-reflow in postischemic skeletal muscle by a mechanism that appears to involve CD18-dependent neutrophil adhesion to the endothelium.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
|
pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
264
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H479-83
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8095375-Animals,
pubmed-meshheading:8095375-Antibodies, Monoclonal,
pubmed-meshheading:8095375-Antigens, CD,
pubmed-meshheading:8095375-Antigens, CD18,
pubmed-meshheading:8095375-Dogs,
pubmed-meshheading:8095375-Female,
pubmed-meshheading:8095375-Ischemia,
pubmed-meshheading:8095375-Male,
pubmed-meshheading:8095375-Muscles,
pubmed-meshheading:8095375-Neutrophils,
pubmed-meshheading:8095375-Receptors, Leukocyte-Adhesion,
pubmed-meshheading:8095375-Regional Blood Flow,
pubmed-meshheading:8095375-Reperfusion,
pubmed-meshheading:8095375-Vascular Patency
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pubmed:year |
1993
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pubmed:articleTitle |
CD18-dependent adherence reactions play an important role in the development of the no-reflow phenomenon.
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pubmed:affiliation |
Department of Physiology, Louisiana State University Medical Center, School of Medicine, Shreveport 71130.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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