<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Maruyama M</submitter><funding>NHLBI NIH HHS</funding><pagination>399-408</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2818796</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>106(2)</volume><pubmed_abstract>&lt;h4>Rationale&lt;/h4>Recurrent ventricular arrhythmias after initial successful defibrillation are associated with poor clinical outcome.&lt;h4>Objective&lt;/h4>We tested the hypothesis that postshock arrhythmias occur because of spontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity (TA) from tissues with high sensitivity of resting membrane voltage (V(m)) to elevated intracellular calcium (Ca(i)) (high diastolic Ca(i)-voltage coupling gains).&lt;h4>Methods and results&lt;/h4>We simultaneously mapped Ca(i) and V(m) on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Ca(i) elevation (SCaE) was noted after defibrillation in 32% of ventricular tachycardia/ventricular fibrillation at baseline and in 81% </pubmed_abstract><journal>Circulation research</journal><pubmed_title>Diastolic intracellular calcium-membrane voltage coupling gain and postshock arrhythmias: role of purkinje fibers and triggered activity.</pubmed_title><pmcid>PMC2818796</pmcid><funding_grant_id>R01 HL071140-06</funding_grant_id><funding_grant_id>R01 HL071140-03</funding_grant_id><funding_grant_id>R01 HL071140-04</funding_grant_id><funding_grant_id>R01 HL071140-01</funding_grant_id><funding_grant_id>R01 HL078932</funding_grant_id><funding_grant_id>R01 HL071140-02</funding_grant_id><funding_grant_id>R01 HL071140-05A1</funding_grant_id><funding_grant_id>P01 HL78931</funding_grant_id><funding_grant_id>R01 HL071140</funding_grant_id><funding_grant_id>P01 HL078931-020003</funding_grant_id><funding_grant_id>R01 HL78932</funding_grant_id><funding_grant_id>R01 HL078932-02</funding_grant_id><funding_grant_id>R01 HL078932-01</funding_grant_id><funding_grant_id>R01 HL71140</funding_grant_id><funding_grant_id>R01 HL078932-04</funding_grant_id><funding_grant_id>R01 HL078932-03</funding_grant_id><funding_grant_id>P01 HL078931-050003</funding_grant_id><funding_grant_id>P01 HL078931</funding_grant_id><funding_grant_id>P01 HL078931-040003</funding_grant_id><funding_grant_id>R01 HL071140-07S1</funding_grant_id><funding_grant_id>R01 HL071140-06S1</funding_grant_id><funding_grant_id>R01 HL078932-05A1</funding_grant_id><funding_grant_id>P01 HL078931-030003</funding_grant_id><funding_grant_id>R01 HL071140-07</funding_grant_id><funding_grant_id>P01 HL078931-01A10003</funding_grant_id><pubmed_authors>Joung B</pubmed_authors><pubmed_authors>Kim DH</pubmed_authors><pubmed_authors>Shen MJ</pubmed_authors><pubmed_authors>Choi EK</pubmed_authors><pubmed_authors>Tang L</pubmed_authors><pubmed_authors>Shinohara T</pubmed_authors><pubmed_authors>Maruyama M</pubmed_authors><pubmed_authors>On YK</pubmed_authors><pubmed_authors>Weiss JN</pubmed_authors><pubmed_authors>Lin SF</pubmed_authors><pubmed_authors>Han S</pubmed_authors><pubmed_authors>Chen PS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Diastolic intracellular calcium-membrane voltage coupling gain and postshock arrhythmias: role of purkinje fibers and triggered activity.</name><description>&lt;h4>Rationale&lt;/h4>Recurrent ventricular arrhythmias after initial successful defibrillation are associated with poor clinical outcome.&lt;h4>Objective&lt;/h4>We tested the hypothesis that postshock arrhythmias occur because of spontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity (TA) from tissues with high sensitivity of resting membrane voltage (V(m)) to elevated intracellular calcium (Ca(i)) (high diastolic Ca(i)-voltage coupling gains).&lt;h4>Methods and results&lt;/h4>We simultaneously mapped Ca(i) and V(m) on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Ca(i) elevation (SCaE) was noted after defibrillation in 32% of ventricular tachycardia/ventricular fibrillation at baseline and in 81% </description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Feb</publication><modification>2025-05-31T23:56:52.139Z</modification><creation>2025-05-31T23:56:52.139Z</creation></dates><accession>S-EPMC2818796</accession><cross_references><pubmed>19926871</pubmed><doi>10.1161/circresaha.109.211292</doi><doi>10.1161/CIRCRESAHA.109.211292</doi></cross_references></HashMap>