Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1984-4-24
pubmed:abstractText
Studies in ischemic canine left ventricle have shown that the depletion of membrane phospholipids is a critical event in the development of a sarcolemmal calcium permeability defect and associated irreversible myocyte injury. The mechanism of phospholipid loss is unclear, but may be due to the activation of endogenous phospholipases. Since arachidonic acid is a fatty acid found almost entirely in phospholipid, increases in arachidonate provide evidence for increased phospholipase activity. The present study was designed to examine the temporal relationship of the accumulation of free arachidonate with the onset of phospholipid depletion during fixed ligation of the left anterior descending coronary artery in canine myocardium. The following results were demonstrated in ischemic canine myocardium: (1) the accumulation of unesterified arachidonate is minimal during 10-30 minutes of ischemia, but is significantly increased after prolonging the duration of ischemia to 1-3 hours; (2) significant increases in arachidonate precede the development of a significant decrease in total phospholipid content; (3) the decrease in the arachidonate content of phosphatidylcholine is accompanied by similar decreases in all of the fatty acyl moieties; (4) the arachidonate content of lysophosphatidylcholine and diacylglycerol are unchanged during myocardial ischemia; (5) there is evidence of a deacylation-reacylation cycle in phosphatidylcholine prior to the accumulation of free arachidonate; (6) the fatty acyl specificity of the lysophosphatidylcholine acyltransferase corresponds to the pattern of fatty acyl remodeling of phosphatidylcholine during early myocardial ischemia. These data suggest that the accumulation of arachidonate may be a more sensitive measure of phospholipid degradation than the decrease in total phospholipid content in ischemic canine myocardium. It is postulated that the defective reacylation of arachidonate into phosphatidylcholine may contribute to the net loss of membrane phospholipid during myocardial ischemia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
313-22
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Accumulation of unesterified arachidonic acid in ischemic canine myocardium. Relationship to a phosphatidylcholine deacylation-reacylation cycle and the depletion of membrane phospholipids.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't