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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1982-12-18
pubmed:abstractText
In an effort to determine the manner in which hypotension following experimental coronary occlusion affects myocardial infarct size, the left anterior descending coronary artery was occluded in 22 barbiturate anaesthetised dogs, the chest was closed, and the dogs allowed to recover. Thirty minutes following coronary occlusion, seven dogs were haemorrhaged to a mean arterial pressure of 8.2 +/- 0.3 kPa (62 +/- 2 mmHg) and maintained at this pressure; no intervention was undertaken in control dogs. Twenty-four hours after coronary occlusion infarct size in control and hypotensive animals was determined. The hypotensive group developed larger percentages of necrosis of the left ventricles distal to the site of occlusion than did the control dogs (37.8 +/- 2.3 vs 30.4 +/- 1.4 (P less than 0.01)). Although the percentage of infarcted endocardium did not change significantly, the infarction of epicardium was 45% larger in the hypotensive group (34.4 +/- 3.3% vs 23.7 +/- 1.9%, P less than 0.01). Regional myocardial blood flow (RMBF) was determined by means of radioactive microspheres in 5 dogs following coronary occlusion before and after hypotension. RMBF following haemorrhage fell by an equal proportion, 61.9 +/- 3.3% in normal tissue and 61.2 +/- 2.4% in ischaemic zones. In conclusion, hypotension caused infarct extension into the epicardium, ie, into tissue that does not become necrotic under control conditions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0008-6363
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
423-7
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Extension of myocardial necrosis into normal epicardium followng hypotension during experimental coronary occlusion.
pubmed:publicationType
Journal Article