{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,15]],"date-time":"2023-10-15T05:11:20Z","timestamp":1697346680779},"reference-count":53,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,5,4]],"date-time":"2007-05-04T00:00:00Z","timestamp":1178236800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,5,15]]},"abstract":"<jats:p>Clinical hypokalaemia is associated with acquired electrocardiographic QT prolongation and arrhythmic activity initiated by premature ventricular depolarizations and suppressed by lidocaine (lignocaine). Nevertheless, regular (S1) pacing at a 125 ms interstimulus interval resulted in stable waveforms and rhythm studied using epicardial and endocardial monophasic action potential (MAP) electrodes in Langendorff\u2010perfused murine hearts whether under normokalaemic (5.2 m<jats:sc>m<\/jats:sc> K<jats:sup>+<\/jats:sup>) or hypokalaemic (3.0 m<jats:sc>m<\/jats:sc> K<jats:sup>+<\/jats:sup>) conditions, in both the presence and absence of lidocaine (10 \u03bc<jats:sc>m<\/jats:sc>). Furthermore, the transmural gradient in repolarization time, known to be altered in the congenital long\u2010QT syndromes, and reflected in the difference between endocardial and epicardial MAP duration at 90% repolarization (\u0394APD<jats:sub>90<\/jats:sub>), did not differ significantly (<jats:italic>P<\/jats:italic> &gt; 0.05) between normokalaemic (5.5 \u00b1 4.5 ms, <jats:italic>n<\/jats:italic>= 8, five hearts), hypokalaemic (<jats:italic>n<\/jats:italic>= 8, five hearts), or lidocaine\u2010treated normokalaemic (<jats:italic>n<\/jats:italic>= 8, five hearts) or hypokalaemic (<jats:italic>n<\/jats:italic>= 8, five hearts) hearts. However, premature ventricular depolarizations occurring in response to extrasystolic (S2) stimulation delivered at S1S2 intervals between 0 and 22 \u00b1 6 ms following recovery from refractoriness initiated arrhythmic activity specifically in hypokalaemic (<jats:italic>n<\/jats:italic>= 8, five hearts) as opposed to normokalaemic (<jats:italic>n<\/jats:italic>= 25, 14 hearts), or lidocaine\u2010treated hypokalaemic (<jats:italic>n<\/jats:italic>= 8, five hearts) or normokalaemic hearts (<jats:italic>n<\/jats:italic>= 8, five hearts). This was associated with sharp but transient reversals in \u0394APD<jats:sub>90<\/jats:sub> in MAPs initiated within the 250 ms interval directly succeeding premature ventricular depolarizations, from 3.3 \u00b1 5.6 ms to \u221231.8 \u00b1 11.8 ms (<jats:italic>P<\/jats:italic> &lt; 0.05) when they were initiated immediately after recovery from refractoriness. In contrast the corresponding latency differences consistently remained close to the normokalaemic value (\u22121.6 \u00b1 1.4 ms, <jats:italic>P<\/jats:italic> &gt; 0.05). These findings empirically associate arrhythmogenesis in hypokalaemic hearts with transient alterations in transmural repolarization gradients resulting from premature ventricular depolarizations. This is in contrast to sustained alterations in transmural repolarization gradients present on regular stimulation in long\u2010QT syndrome models.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.128637","type":"journal-article","created":{"date-parts":[[2007,3,2]],"date-time":"2007-03-02T03:56:11Z","timestamp":1172807771000},"page":"277-289","source":"Crossref","is-referenced-by-count":13,"title":["Transient alterations in transmural repolarization gradients and arrhythmogenicity in hypokalaemic Langendorff\u2010perfused murine hearts"],"prefix":"10.1113","volume":"581","author":[{"given":"Ian N.","family":"Sabir","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew J.","family":"Killeen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Catharine 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