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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-12-5
pubmed:abstractText
We investigated the mechanisms of increase in the pulmonary vascular permeability, focusing on the changes in the peripheral white blood cell (WBC) counts and the surface expression of CD18 on polymorphonuclear cells (PMNs). Anesthetized sheep with chronic lung lymph fistulas were used in this study. We infused synthetic endotoxin (LPS) at a rate of 10 ng/kg/min (i.v.) continuously for 24 hr. We measured lung lymph flow, lymph-to-plasma protein concentration ratio and WBC counts in blood and lung lymph, and the PMNs' surface expression of CD18 before and at 2, 10 and 24 hr after the start of endotoxin infusion, respectively. CD18 was analyzed by flow cytometry using monoclonal anti-CD18 antibody. We found that the pulmonary vascular permeability increased during 2-4 hr after the start of endotoxin infusion, and returned to the baseline over 10 hr. At time 2 hr period, the number of WBCs in the lung lymph increased, the number of peripheral WBCs, mostly PMNs, decreased and the surface expression of CD18 on the peripheral PMNs was up-regulated. At time 10 and 24 hr, the number of WBCs in lung lymph decreased, the number of peripheral WBCs increased and CD18 expression was down-regulated. These data indicate that up-regulation of CD18 expression promotes the PMN adherence to the pulmonary endothelium, migration into the lung and increases the pulmonary vascular permeability. We conclude that the continuous endotoxin infusion up-regulates CD18, which contributes to the PMN migration into the lung.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0040-8727
pubmed:author
pubmed:issnType
Print
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
213-22
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Adhesion molecule CD18 on polymorphonuclear cells correlates to the lung injury caused by continuous infusion of endotoxin in sheep.
pubmed:affiliation
Department of Thoracic Surgery, Tohoku University, Sendai.
pubmed:publicationType
Journal Article