dc.creator | Mattiazzi, Ramona Alicia | |
dc.creator | Argenziano, Mariana Alejandra | |
dc.creator | Aguilar-Sanchez, Yuriana | |
dc.creator | Mazzocchi, Gabriela | |
dc.creator | Escobar, Ariel L. | |
dc.date.accessioned | 2018-03-05T18:46:44Z | |
dc.date.available | 2018-03-05T18:46:44Z | |
dc.date.created | 2018-03-05T18:46:44Z | |
dc.date.issued | 2015-02 | |
dc.identifier | Mattiazzi, Ramona Alicia; Argenziano, Mariana Alejandra; Aguilar-Sanchez, Yuriana; Mazzocchi, Gabriela; Escobar, Ariel L.; Ca2+ Sparks and Ca2+ waves are the subcellular events underlying Ca2+ overload during ischemia and reperfusion in perfused intact hearts; Academic Press Ltd - Elsevier Science Ltd; Journal of Molecular and Cellular Cardiology; 79; 2-2015; 69-78 | |
dc.identifier | 0022-2828 | |
dc.identifier | http://hdl.handle.net/11336/37807 | |
dc.identifier | CONICET Digital | |
dc.identifier | CONICET | |
dc.description.abstract | Abnormal intracellular Ca2+ cycling plays a key role in cardiac dysfunction, particularly during the setting of ischemia/reperfusion (I/R). During ischemia, there is an increase in cytosolic and sarcoplasmic reticulum (SR) Ca2+. At the onset of reperfusion, there is a transient and abrupt increase in cytosolic Ca2++, which occurs timely associated with reperfusion arrhythmias. However, little is known about the subcellular dynamics of Ca2+ increase during I/R, and a possible role of the SR as a mechanism underlying this increase has been previously overlooked. The aim of the present work is to test two main hypotheses: (1) An increase diastolic Ca2+ sparks frequency (cspf) constitutes a mayor substrate for the ischemia-induced diastolic Ca2+ increase; (2) an increase in cytosolic Ca2+ pro-arrhythmogenic events (Ca2+ waves), mediates the abrupt diastolic Ca2+ rise at the onset of reperfusion. We used confocal microscopy on mouse intact hearts loaded with Fluo-4. Hearts were submitted to global I/R (12/30min) to assess epicardial Ca2+ sparks in the whole heart. Intact heart sparks were faster than in isolated myocytes whereas cspf was not different. During ischemia, cspf significantly increased relative to preischemia (2.07±0.33 vs. 1.13±0.20 sp/s/100μm, n=29/34, 7 hearts). Reperfusion significantly changed Ca2+ sparks kinetics, by prolonging Ca2+ sparks rise time and decreased cspf. However, it significantly increased Ca2+ wave frequency relative to ischemia (0.71±0.14 vs. 0.38±0.06 w/s/100μm, n=32/33, 7 hearts). The results show for the first time the assessment of intact perfused heart Ca2+ sparks and provides direct evidence of increased Ca2+ sparks in ischemia that transform into Ca2+ waves during reperfusion. These waves may constitute a main trigger for reperfusion arrhythmias. | |
dc.language | eng | |
dc.publisher | Academic Press Ltd - Elsevier Science Ltd | |
dc.relation | info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.yjmcc.2014.10.011 | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0022282814003320 | |
dc.rights | https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | Ca2+ Sparks | |
dc.subject | Intact Heart | |
dc.subject | Ischemia/Reperfusion | |
dc.title | Ca2+ Sparks and Ca2+ waves are the subcellular events underlying Ca2+ overload during ischemia and reperfusion in perfused intact hearts | |
dc.type | info:eu-repo/semantics/article | |
dc.type | info:ar-repo/semantics/artículo | |
dc.type | info:eu-repo/semantics/publishedVersion | |