{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T03:50:28Z","timestamp":1792727428496,"version":"4.5.0"},"reference-count":54,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2010,6]]},"abstract":"<jats:p>\n                    Ca\n                    <jats:sup>+<\/jats:sup>\n                    -induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release tightly controls the function of ventricular cardiac myocytes under normal and pathological conditions. Two major factors contributing to the regulation of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release are the cytosolic free Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration and sarcoplasmic reticulum (SR) Ca\n                    <jats:sup>2+<\/jats:sup>\n                    content. We hypothesized that the amount of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    released from the SR during each heart beat strongly defines the refractoriness of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release. To test this hypothesis, EGTA AM, a high-affinity, slow-association rate Ca\n                    <jats:sup>2+<\/jats:sup>\n                    chelator, was used as a tool to modify luminal SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    content. An analysis of the cytosolic and luminal SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    dynamics recorded from the epicardial layer of intact mouse hearts indicated that the presence of EGTA reduced the diastolic SR free Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration and fraction of SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    depletion during each beat. In addition, this maneuver shortened the refractory period and accelerated the restitution of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release. As a consequence of the accelerated restitution, the frequency dependence of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    alternans was significantly shifted toward higher heart rates, suggesting a role of luminal SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    in the genesis of this highly arrhythmogenic phenomenon. Thus, intra-SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    dynamics set the refractoriness and frequency dependence of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    transients in subepicardial ventricular myocytes.\n                  <\/jats:p>","DOI":"10.1152\/ajpheart.00885.2009","type":"journal-article","created":{"date-parts":[[2010,4,9]],"date-time":"2010-04-09T21:52:52Z","timestamp":1270849972000},"page":"H2138-H2153","source":"Crossref","is-referenced-by-count":29,"title":["Luminal Ca\n                    <sup>2+<\/sup>\n                    content regulates intracellular Ca\n                    <sup>2+<\/sup>\n                    release in subepicardial myocytes of intact beating mouse hearts: effect of exogenous buffers"],"prefix":"10.1152","volume":"298","author":[{"given":"Dmytro","family":"Kornyeyev","sequence":"first","affiliation":[{"name":"School of Engineering, University of California, Merced, 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