Linked Life Data

1656913

Source:http://linkedlifedata.com/resource/pubmed/id/1656913

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1991-11-4
pubmed:abstractText
Superoxide radicals are supposed to contribute to myocardial reperfusion injury. Their origin, however, is still a matter of debate. Polymorphonuclear leukocytes (PMNL) have been discussed as a major postischaemic .O2- source [Lucchesi and Mullane (1986) Ann Rev Pharmacol Toxicol 26: 201-224]. We studied the role of .O2- derived from human polymorphonuclear leukocytes in reperfused and normoxic perfused isolated rat hearts. During reperfusion PMNL exerted deleterious effects on different parameters (e.g. contractility, coronary flow) of isolated rat hearts. Under normoxic perfusion conditions stimulation of PMNL with N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) caused bradycardia and a transient vasoconstriction. Superoxide dismutase (SOD) administration did not influence any of the PMNL effects mentioned, suggesting that leukocytic .O2- was not involved in PMNL-induced cardiac dysfunctions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0340-5761
pubmed:author
pubmed:issnType
Print
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
361-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Leukocytic .O2- and cardiac dysfunctions in isolated perfused rat hearts.
pubmed:affiliation
Grünenthal GmbH, Center of Research, Aachen, FRG.
pubmed:publicationType
Journal Article, In Vitro