Linked Life Data

8781538

Source:http://linkedlifedata.com/resource/pubmed/id/8781538

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-10-4
pubmed:abstractText
A burst of endothelial derived oxidants including hydrogen peroxide (H2O2) and superoxide (.O2-) occurs on reperfusion of ischemic tissues that directly causes injury; however, it is not known if this also triggers further injury due to subsequent leukocyte adhesion and adhesion molecule expression. Therefore, studies were performed in an isolated heart model developed to enable study of the role of isolated cellular and humoral factors in the mechanism of postischemic injury. Isolated rat hearts were subjected to 20 min of 37 degrees C-global ischemia followed by reperfusion with polymorphonuclear leukocytes (PMNs) and plasma in the presence or absence of superoxide dismutase (SOD), 200 U/ml, or catalase, 500 U/ml. Measurements of contractile function, coronary flow, high-energy phosphates, free radical generation, and PMN accumulation were performed. Adhesion molecule expression was measured on the surface of effluent PMNs by fluorescence flow cytometry and within the tissue using immunohistochemistry. SOD or catalase treatment resulted in 2- to 3-fold higher recoveries of contractile function, coronary flow, and high energy phosphates. EPR spin trapping measurements demonstrated that SOD totally quenched the free radical generation observed upon reperfusion while catalase prevented the formation of hydroxyl and alkyl radicals derived from superoxide. SOD or catalase treatment decreased PMN accumulation in the reperfused heart and prevented the marked upregulation of CD18 expression seen after reperfusion. These experiments demonstrate that in addition to their direct antioxidative actions, SOD and catalase each decrease PMN adhesion and CD18 expression resulting in marked suppression of PMN-mediated injury in the postischemic heart. Thus, endothelial derived H2O2 and .O2- further amplify postischemic injury by triggering CD18 expression on the surface of PMNs leading to increased PMN adhesion within the heart.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
23
pubmed:volume
1316
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
191-202
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:8781538-Animals, pubmed-meshheading:8781538-Antigens, CD18, pubmed-meshheading:8781538-Antioxidants, pubmed-meshheading:8781538-Catalase, pubmed-meshheading:8781538-Cell Adhesion, pubmed-meshheading:8781538-Coronary Circulation, pubmed-meshheading:8781538-Electron Spin Resonance Spectroscopy, pubmed-meshheading:8781538-Energy Metabolism, pubmed-meshheading:8781538-Female, pubmed-meshheading:8781538-Hemodynamics, pubmed-meshheading:8781538-Humans, pubmed-meshheading:8781538-Hydrogen Peroxide, pubmed-meshheading:8781538-Myocardium, pubmed-meshheading:8781538-Neutrophils, pubmed-meshheading:8781538-Rats, pubmed-meshheading:8781538-Rats, Sprague-Dawley, pubmed-meshheading:8781538-Reperfusion Injury, pubmed-meshheading:8781538-Respiratory Burst, pubmed-meshheading:8781538-Superoxide Dismutase, pubmed-meshheading:8781538-Superoxides
pubmed:year
1996
pubmed:articleTitle
Superoxide and hydrogen peroxide induce CD18-mediated adhesion in the postischemic heart.
pubmed:affiliation
Molecular and Cellular Biophysics Laboratories, Johns Hopkins Medical Institutions, Johns Hopkins Bayview Medical Center, Baltimore, MD 21224, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't