Linked Life Data

9436824

Source:http://linkedlifedata.com/resource/pubmed/id/9436824

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1998-2-17
pubmed:abstractText
Our objective was to investigate the effects of alpha1- or beta-adrenoceptor blockers on endocardial and epicardial refractory-period changes during myocardial ischemia in alpha-chloralose-anesthetized dogs. The first and second diagonal branches of the left anterior descending coronary artery were ligated. The refractory period was determined by an S1-S2 extrastimulus method. Dogs were treated with the alpha1-blocker bunazosin (0.1-0.2 mg/kg, i.v.; n = 16), the beta-blocker propranolol (0.2 mg/kg, i.v.; n = 15), or saline (n = 11). Dogs that developed ventricular tachycardia/fibrillation (VT/VF) during the experiment were excluded from the statistical assessment in refractory periods. In all groups, coronary ligation produced a significant shortening of the refractory period of ischemic epicardial tissue (p < 0.05) but only minimal shortening of ischemic endocardial refractory periods, resulting in an increased difference in repolarization time between the endo- and epicardial sites. Treatment with bunazosin ameliorated this ischemia-related shortening of refractory periods at both the endo- and epicardial sites, with a greater effect seen epicardially (p < 0.05), resulting in values similar to those in the nonischemic tissue. Treatment with propranolol prolonged refractory periods more in the epicardial (p < 0.01) than in endocardial sites, exacerbating the disparity in the refractory period between the endo- and epicardial sites (p < 0.05). Propranolol also prolonged the refractory period of nonischemic tissue (p < 0.05 and p < 0.01 in endo- and epicardial sites, respectively), resulting in a significant difference between the ischemic and normal myocardium at the endocardial site (p < 0.05). Results suggest that the alpha1-blocker bunazosin reduces the refractory-period disparity between the ischemic and normal myocardium without increasing the disparity between the endo- and epicardial surfaces, whereas propranolol produces a greater disparity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
824-30
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9436824-Adrenergic alpha-1 Receptor Antagonists, pubmed-meshheading:9436824-Adrenergic alpha-Antagonists, pubmed-meshheading:9436824-Adrenergic beta-Antagonists, pubmed-meshheading:9436824-Animals, pubmed-meshheading:9436824-Blood Pressure, pubmed-meshheading:9436824-Dogs, pubmed-meshheading:9436824-Endocardium, pubmed-meshheading:9436824-Heart Ventricles, pubmed-meshheading:9436824-Myocardial Ischemia, pubmed-meshheading:9436824-Pericardium, pubmed-meshheading:9436824-Propranolol, pubmed-meshheading:9436824-Quinazolines, pubmed-meshheading:9436824-Receptors, Adrenergic, alpha-1, pubmed-meshheading:9436824-Refractory Period, Electrophysiological, pubmed-meshheading:9436824-Tachycardia, Ventricular, pubmed-meshheading:9436824-Ventricular Fibrillation, pubmed-meshheading:9436824-Ventricular Function
pubmed:year
1997
pubmed:articleTitle
Differences in refractory-period response of canine subendocardium and subepicardium to bunazosin, an alpha1-adrenoceptor antagonist, and propranolol during myocardial ischemia.
pubmed:affiliation
Department of Cardiovascular Medicine, School of Medicine, Tokai University, Isehara, Kanagawa, Japan.
pubmed:publicationType
Journal Article