Linked Life Data

1728431

Source:http://linkedlifedata.com/resource/pubmed/id/1728431

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-2-6
pubmed:abstractText
Coronary occlusion leading to nearly total absence of myocardial perfusion is the major cause of lethal ischemic arrhythmia in humans. In this setting, intracellular acidosis rapidly develops and leads to accelerated K+ efflux from the myocyte. Other metabolites, including lipid amphiphiles such as LPC, also rapidly accumulate in the ischemic zone. Elevated extracellular K+ and LPC cause membrane depolarization, which leads to slow conduction and increased refractoriness. These electrophysiologic changes contribute to the development of re-entrant rhythms, which predominate during early ischemia (phase 1a). Diffusion of extracellular K+ from the ischemic zone and release of endogenous catecholamines result in improvement in electrophysiologic parameters and are associated with a short arrhythmia-free interval, which occurs approximately 10 minutes after coronary occlusion. A second phase of arrhythmia (1b) then occurs and may be due in part to catecholamine-mediated triggered activity. Irreversible cell injury occurs 15 to 20 minutes after coronary occlusion and is associated with cell Ca++ overload, loss of gap junctions, and impaired cell coupling. This may lead to re-entrant arrhythmias. Reperfusion of ischemic myocardium leads to arrhythmia predominantly mediated by non re-entrant mechanisms. In humans, these reperfusion arrhythmias are usually relatively benign.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0069-0384
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3-18
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Mechanisms of ventricular arrhythmias in acute ischemia and reperfusion.
pubmed:publicationType
Journal Article, Review