Electrophysiologic properties of a narrow isthmus in rabbit atrial tissue: cycle length dependent effect of quinidine.
Identifieur interne : 004124 ( Main/Exploration ); précédent : 004123; suivant : 004125Electrophysiologic properties of a narrow isthmus in rabbit atrial tissue: cycle length dependent effect of quinidine.
Auteurs : A. Qi [Canada] ; C R Kerr ; J A Yeung-Lai-WahSource :
- Canadian journal of physiology and pharmacology [ 0008-4212 ] ; 1994.
English descriptors
- KwdEn :
- Action Potentials (drug effects), Animals, Atrial Function, Cardiac Pacing, Artificial, Electrophysiology, Heart (drug effects), Heart (physiology), Heart Atria (drug effects), In Vitro Techniques, Neural Conduction (physiology), Quinidine (pharmacology), Rabbits, Refractory Period, Electrophysiological (drug effects).
- MESH :
- chemical , pharmacology : Quinidine.
- drug effects : Action Potentials, Heart, Heart Atria, Refractory Period, Electrophysiological.
- physiology : Heart, Neural Conduction.
- Animals, Atrial Function, Cardiac Pacing, Artificial, Electrophysiology, In Vitro Techniques, Rabbits.
Abstract
The modulation of quinidine's effect by pacing cycle lengths was assessed over an isthmus of atrial myocardium, simulating the Wolff-Parkinson-White syndrome. Isolated rabbit atria were dissected so that two tissue blocks, A and B, were linked by an isthmus, 1 mm in width. Effective refractory period in the tissue blocks and over the isthmus was measured at cycle lengths of 1,000, 600, and 400 ms, and the minimum cycle length to sustain 1:1 conduction over the isthmus was measured before treatment, during quinidine superfusion (4 mg/L), and after washout. Longitudinal velocity over the isthmus was also measured. The increment in the effective refractory period in the tissue blocks by quinidine appeared to be similar, about 10% at three pacing cycle lengths (p > 0.05). However, the increment of the effective refractory period over the isthmus was modulated by pacing cycle lengths: greater increase at shorter cycle lengths (p < 0.001). Quinidine prolonged the minimum cycle length over the isthmus by 44 +/- 17%. Regression analysis showed that after quinidine there was a correlationship between conduction velocity and refractoriness over the isthmus (R = 0.85, p < 0.001). Intracellular implements showed stable action potentials, confirming the integrity of the preparation. We conclude that (i) quinidine preferentially prolongs refractoriness over the isthmus and (ii) quinidine's effect on refractoriness over the isthmus is cycle length dependent.
PubMed: 7922869
Affiliations:
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Qi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Cardiology, University Hospital, UBC Site, University of British Columbia, Vancouver, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medicine, Cardiology, University Hospital, UBC Site, University of British Columbia, Vancouver</wicri:regionArea><wicri:noRegion>Vancouver</wicri:noRegion></affiliation></author><author><name sortKey="Kerr, C R" sort="Kerr, C R" uniqKey="Kerr C" first="C R" last="Kerr">C R Kerr</name></author><author><name sortKey="Yeung Lai Wah, J A" sort="Yeung Lai Wah, J A" uniqKey="Yeung Lai Wah J" first="J A" last="Yeung-Lai-Wah">J A Yeung-Lai-Wah</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1994">1994</date><idno type="RBID">pubmed:7922869</idno><idno type="pmid">7922869</idno><idno type="wicri:Area/PubMed/Corpus">001974</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001974</idno><idno type="wicri:Area/PubMed/Curation">001974</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001974</idno><idno type="wicri:Area/PubMed/Checkpoint">001974</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001974</idno><idno type="wicri:Area/Ncbi/Merge">002430</idno><idno type="wicri:Area/Ncbi/Curation">002430</idno><idno type="wicri:Area/Ncbi/Checkpoint">002430</idno><idno type="wicri:doubleKey">0008-4212:1994:Qi A:electrophysiologic:properties:of</idno><idno type="wicri:Area/Main/Merge">004874</idno><idno type="wicri:Area/Main/Curation">004124</idno><idno type="wicri:Area/Main/Exploration">004124</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Electrophysiologic properties of a narrow isthmus in rabbit atrial tissue: cycle length dependent effect of quinidine.</title><author><name sortKey="Qi, A" sort="Qi, A" uniqKey="Qi A" first="A" last="Qi">A. Qi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Cardiology, University Hospital, UBC Site, University of British Columbia, Vancouver, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medicine, Cardiology, University Hospital, UBC Site, University of British Columbia, Vancouver</wicri:regionArea><wicri:noRegion>Vancouver</wicri:noRegion></affiliation></author><author><name sortKey="Kerr, C R" sort="Kerr, C R" uniqKey="Kerr C" first="C R" last="Kerr">C R Kerr</name></author><author><name sortKey="Yeung Lai Wah, J A" sort="Yeung Lai Wah, J A" uniqKey="Yeung Lai Wah J" first="J A" last="Yeung-Lai-Wah">J A Yeung-Lai-Wah</name></author></analytic><series><title level="j">Canadian journal of physiology and pharmacology</title><idno type="ISSN">0008-4212</idno><imprint><date when="1994" type="published">1994</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action Potentials (drug effects)</term><term>Animals</term><term>Atrial Function</term><term>Cardiac Pacing, Artificial</term><term>Electrophysiology</term><term>Heart (drug effects)</term><term>Heart (physiology)</term><term>Heart Atria (drug effects)</term><term>In Vitro Techniques</term><term>Neural Conduction (physiology)</term><term>Quinidine (pharmacology)</term><term>Rabbits</term><term>Refractory Period, Electrophysiological (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Quinidine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Action Potentials</term><term>Heart</term><term>Heart Atria</term><term>Refractory Period, Electrophysiological</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Heart</term><term>Neural Conduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Atrial Function</term><term>Cardiac Pacing, Artificial</term><term>Electrophysiology</term><term>In Vitro Techniques</term><term>Rabbits</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The modulation of quinidine's effect by pacing cycle lengths was assessed over an isthmus of atrial myocardium, simulating the Wolff-Parkinson-White syndrome. Isolated rabbit atria were dissected so that two tissue blocks, A and B, were linked by an isthmus, 1 mm in width. Effective refractory period in the tissue blocks and over the isthmus was measured at cycle lengths of 1,000, 600, and 400 ms, and the minimum cycle length to sustain 1:1 conduction over the isthmus was measured before treatment, during quinidine superfusion (4 mg/L), and after washout. Longitudinal velocity over the isthmus was also measured. The increment in the effective refractory period in the tissue blocks by quinidine appeared to be similar, about 10% at three pacing cycle lengths (p > 0.05). However, the increment of the effective refractory period over the isthmus was modulated by pacing cycle lengths: greater increase at shorter cycle lengths (p < 0.001). Quinidine prolonged the minimum cycle length over the isthmus by 44 +/- 17%. Regression analysis showed that after quinidine there was a correlationship between conduction velocity and refractoriness over the isthmus (R = 0.85, p < 0.001). Intracellular implements showed stable action potentials, confirming the integrity of the preparation. We conclude that (i) quinidine preferentially prolongs refractoriness over the isthmus and (ii) quinidine's effect on refractoriness over the isthmus is cycle length dependent.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Kerr, C R" sort="Kerr, C R" uniqKey="Kerr C" first="C R" last="Kerr">C R Kerr</name><name sortKey="Yeung Lai Wah, J A" sort="Yeung Lai Wah, J A" uniqKey="Yeung Lai Wah J" first="J A" last="Yeung-Lai-Wah">J A Yeung-Lai-Wah</name></noCountry><country name="Canada"><noRegion><name sortKey="Qi, A" sort="Qi, A" uniqKey="Qi A" first="A" last="Qi">A. 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