Linked Life Data

1605027

Source:http://linkedlifedata.com/resource/pubmed/id/1605027

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-7-14
pubmed:abstractText
The effects of cimetidine (Cim) on ventricular fibrillation threshold (VFT), diastolic excitation threshold (DET), effective refractory period (ERP), and vulnerable period (VP), were determined in both stable perfusion and postischemic reperfusion rat hearts. The results showed that reperfusion after 15 min global myocardial ischemia caused a significant decrease VFT and ERP, and an increase in VP and DET. Cim 1 mmol.L-1 prevented the lowering in VFT, shortening in ERP, and lengthening in VP from the postischemic reperfusion. Cim 0.1 mmol.L-1 attenuated the exacerbation of VFT and VP. Cim 0.01 mmol.L-1 did not exert any noticeable influence on the electrophysiological parameters. It was shown that Cim 1 mmol.L-1 protected myocardium against the aggravation of electrophysiological characteristics induced by postischemic reperfusion.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0253-9756
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Effect of cimetidine on isolated rat myocardial reperfusion injury.
pubmed:affiliation
Department of Physiology, Zhejiang Medical University, Hangzhou, China.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't