Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2005-3-4
pubmed:abstractText
Action potential duration (APD) restitution properties and repolarization alternans are thought to be important arrhythmogenic factors. We investigated the role of intracellular calcium (Ca2+i) cycling in regulating APD restitution slope and repolarization (APD) alternans in patch-clamped rabbit ventricular myocytes at 34 to 36 degrees C, using the perforated or ruptured patch clamp techniques with Fura-2-AM to record Ca2+i. When APD restitution was measured by either the standard extrastimulus (S1S2) method or the dynamic rapid pacing method, the maximum APD restitution slope exceeded 1 by both methods, but was more shallow with the dynamic method. These differences were associated with greater Ca2+i accumulation during dynamic pacing. The onset of APD alternans occurred at diastolic intervals at which the APD restitution slope was significantly <1 and was abolished by suppressing sarcoplasmic reticulum (SR) Ca2+i cycling with thapsigargin and ryanodine, or buffering the global Ca2+i transient with BAPTA-AM or BAPTA. Thapsigargin and ryanodine flattened APD restitution slope to <1 when measured by the dynamic method, but not by the S1S2 method. BAPTA-AM or BAPTA failed to flatten APD restitution slope to <1 by either method. In conclusion, APD alternans requires intact Ca2+i cycling and is not reliably predicted by APD restitution slope when Ca2+i cycling is suppressed. Ca2+i cycling may contribute to differences between APD restitution curves measured by S1S2 versus dynamic pacing protocols by inducing short-term memory effects related to pacing-dependent Ca2+i accumulation.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
4
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
459-66
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15662034-Action Potentials, pubmed-meshheading:15662034-Animals, pubmed-meshheading:15662034-Caffeine, pubmed-meshheading:15662034-Calcium, pubmed-meshheading:15662034-Calcium Channels, pubmed-meshheading:15662034-Calcium Channels, L-Type, pubmed-meshheading:15662034-Calcium Signaling, pubmed-meshheading:15662034-Cardiac Pacing, Artificial, pubmed-meshheading:15662034-Cells, Cultured, pubmed-meshheading:15662034-Egtazic Acid, pubmed-meshheading:15662034-Heart Conduction System, pubmed-meshheading:15662034-Humans, pubmed-meshheading:15662034-Ion Transport, pubmed-meshheading:15662034-Models, Cardiovascular, pubmed-meshheading:15662034-Myocardium, pubmed-meshheading:15662034-Myocytes, Cardiac, pubmed-meshheading:15662034-Patch-Clamp Techniques, pubmed-meshheading:15662034-Rabbits, pubmed-meshheading:15662034-Ryanodine, pubmed-meshheading:15662034-Sarcoplasmic Reticulum, pubmed-meshheading:15662034-Tachycardia, Ventricular, pubmed-meshheading:15662034-Thapsigargin, pubmed-meshheading:15662034-Time Factors
pubmed:year
2005
pubmed:articleTitle
Action potential duration restitution and alternans in rabbit ventricular myocytes: the key role of intracellular calcium cycling.
pubmed:affiliation
UCLA Cardiovascular Research Laboratory, Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, Los Angeles, Calif 90095-1679, USA. jgoldhaber@mednet.ucla.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural