pubmed-article:8014865 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8014865 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:8014865 | lifeskim:mentions | umls-concept:C0085979 | lld:lifeskim |
pubmed-article:8014865 | lifeskim:mentions | umls-concept:C1522565 | lld:lifeskim |
pubmed-article:8014865 | lifeskim:mentions | umls-concept:C0002598 | lld:lifeskim |
pubmed-article:8014865 | lifeskim:mentions | umls-concept:C0214230 | lld:lifeskim |
pubmed-article:8014865 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
pubmed-article:8014865 | lifeskim:mentions | umls-concept:C1533157 | lld:lifeskim |
pubmed-article:8014865 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:8014865 | pubmed:dateCreated | 1994-7-26 | lld:pubmed |
pubmed-article:8014865 | pubmed:abstractText | We examined the effects of amiodarone (5-20 microM) on both whole-cell inward rectifier potassium current (IK1) and single IK1 channel activity in isolated guinea pig ventricular myocytes using patch-clamp techniques. In whole-cell voltage-clamp experiments (n = 8), amiodarone (10-20 microM) caused only a small reduction of outward current at -50 mV (12 +/- 6%, no significant difference, N.S.). However, inward current was significantly reduced at -120 mV (21 +/- 7%; P < .05). When CdCl2 (100 microM) and tetrodotoxin (10 microM) were used to block inward Ca++ and Na+ current, respectively, amiodarone significantly reduced IK1 in both the inward (14 +/- 5% at -120 mV; P < .02) and outward (12 +/- 5% at -50 mV; P < .05; n = 11) directions. However, block required high drug concentrations (10-20 microM) and was slow in onset. In contrast, amiodarone did not affect membrane current when IK1 had been previously blocked by Ba++ (5 mM). In inside-out patch-clamp experiments, amiodarone (5 microM) reduced single IK1 channel open probability by increasing interburst interval (from 0.6 +/- 0.03 to 3.1 +/- 0.9 sec; n = 5; P < .05) with no significant difference in the duration of mean open and closed times or the number of shut events within a burst. The net result was that there was only a small change in both burst duration and single-channel kinetics within a burst. Complete channel block occurred after the increase in interburst interval (n = 6 of six cells).(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
pubmed-article:8014865 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:language | eng | lld:pubmed |
pubmed-article:8014865 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8014865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8014865 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8014865 | pubmed:month | Jun | lld:pubmed |
pubmed-article:8014865 | pubmed:issn | 0022-3565 | lld:pubmed |
pubmed-article:8014865 | pubmed:author | pubmed-author:SatoRR | lld:pubmed |
pubmed-article:8014865 | pubmed:author | pubmed-author:HisatomiMM | lld:pubmed |
pubmed-article:8014865 | pubmed:author | pubmed-author:SingerD HDH | lld:pubmed |
pubmed-article:8014865 | pubmed:author | pubmed-author:WasserstromJ... | lld:pubmed |
pubmed-article:8014865 | pubmed:author | pubmed-author:KoumiSS | lld:pubmed |
pubmed-article:8014865 | pubmed:author | pubmed-author:JilGG | lld:pubmed |
pubmed-article:8014865 | pubmed:author | pubmed-author:EagerSS | lld:pubmed |
pubmed-article:8014865 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8014865 | pubmed:volume | 269 | lld:pubmed |
pubmed-article:8014865 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8014865 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8014865 | pubmed:pagination | 1213-9 | lld:pubmed |
pubmed-article:8014865 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:8014865 | pubmed:meshHeading | pubmed-meshheading:8014865-... | lld:pubmed |
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pubmed-article:8014865 | pubmed:meshHeading | pubmed-meshheading:8014865-... | lld:pubmed |
pubmed-article:8014865 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:8014865 | pubmed:articleTitle | Amiodarone blocks the inward rectifier potassium channel in isolated guinea pig ventricular cells. | lld:pubmed |
pubmed-article:8014865 | pubmed:affiliation | Reingold ECG Center, Department of Medicine, Northwestern University Medical School, Chicago, Illinois. | lld:pubmed |
pubmed-article:8014865 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8014865 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:8014865 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:8014865 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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