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pubmed-article:2004404rdf:typepubmed:Citationlld:pubmed
pubmed-article:2004404lifeskim:mentionsumls-concept:C0027051lld:lifeskim
pubmed-article:2004404lifeskim:mentionsumls-concept:C0681814lld:lifeskim
pubmed-article:2004404pubmed:issue5lld:pubmed
pubmed-article:2004404pubmed:dateCreated1991-4-25lld:pubmed
pubmed-article:2004404pubmed:abstractTextA total of 31 dogs were investigated with the aim to evaluate possibilities of pharmacological reduction of ischaemic perfusion damage of the heart muscle. In the experiment two-hour complete ischaemia was used (ligature of the ramus interventricularis anterior) and a subsequent two-hour period of reperfusion. The magnitude of the infarction focus evaluated as the percentage of the ischaemic risk area, using the triphenyltetrazolium method, extended by colour detection of collaterals, was evaluated. Furthermore the authors also evaluated the prevalence of ventricular dysrhythmias in the reperfusion period. In a group of 10 dogs treated by N-acetylcysteine, 100 mg per kg body weight, the authors revealed on comparison with 11 dogs of the control group a diminution of the infarction focus by 32.7%. By addition of Panthenol, 50 mg/kg to N-acetylcysteine in another 10 dogs, a diminution of the infarction by 49% was achieved. The magnitude of the infarction focus was 55.0 +/- 7.0% in the control group, 37.0 +/- 12.6% in dogs treated with N-acetylcysteine (p less than 0.01) and 28.0 +/- 13.3% after administration of N-acetylcysteine and Panthenol (p, as compared with control, again less than 0.01). N-acetylcysteine reduces also significantly the prevalence of ventricular dysrhythmias in the reperfusion period. As compared with the control group this difference is most marked after 60 minutes have elapsed following release of the ligature (p less than 0.001).lld:pubmed
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pubmed-article:2004404pubmed:statusMEDLINElld:pubmed
pubmed-article:2004404pubmed:monthFeblld:pubmed
pubmed-article:2004404pubmed:issn0008-7335lld:pubmed
pubmed-article:2004404pubmed:authorpubmed-author:VránaMMlld:pubmed
pubmed-article:2004404pubmed:authorpubmed-author:KolbKKlld:pubmed
pubmed-article:2004404pubmed:authorpubmed-author:SochmanJJlld:pubmed
pubmed-article:2004404pubmed:issnTypePrintlld:pubmed
pubmed-article:2004404pubmed:day1lld:pubmed
pubmed-article:2004404pubmed:volume130lld:pubmed
pubmed-article:2004404pubmed:ownerNLMlld:pubmed
pubmed-article:2004404pubmed:authorsCompleteYlld:pubmed
pubmed-article:2004404pubmed:pagination139-43lld:pubmed
pubmed-article:2004404pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:2004404pubmed:meshHeadingpubmed-meshheading:2004404-...lld:pubmed
pubmed-article:2004404pubmed:year1991lld:pubmed
pubmed-article:2004404pubmed:articleTitle[Possibilities of limiting myocardial infarct in an experiment].lld:pubmed
pubmed-article:2004404pubmed:affiliationInstitut klinické a experimentální medicíny, Praha.lld:pubmed
pubmed-article:2004404pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:2004404pubmed:publicationTypeEnglish Abstractlld:pubmed