| dc.creator | Valverde, Carlos Alfredo | |
| dc.creator | Kornyeyev, Dmytro | |
| dc.creator | Mattiazzi, Alicia Ramona | |
| dc.creator | Escobar, Ariel L. | |
| dc.date | 2009 | |
| dc.date | 2022-07-11T17:38:53Z | |
| dc.date.accessioned | 2023-07-15T04:48:52Z | |
| dc.date.available | 2023-07-15T04:48:52Z | |
| dc.identifier | http://sedici.unlp.edu.ar/handle/10915/139279 | |
| dc.identifier | issn:0006-3495 | |
| dc.identifier | issn:1542-0086 | |
| dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/7470983 | |
| dc.description | After a brief ischemic insult, a sustained contractile dysfunction occurs manifested as a sluggish recovery of pump function (myocardial stunning). Substantial evidence supports that myocardial dysfunction is triggered by Ca2+ overload during reperfusion (R). Previous results from different laboratories including our own, describe a cascade of events triggered by R that involves the activation of Na+/H+ and Na+/Ca2+ (NCX) exchangers, with enhanced Ca2+ influx. Whether this Ca2+ influx directly produces the increase in cytosolic Ca2+ or this increase occurs as a consequence of sarcoplasmic reticulum (SR) Ca2+ release triggered in turn by the Ca2+ influx, is not known. To address this issue, we performed 12 min of global no-flow ischemia followed by R in the isovolumic Langendorff perfused mouse heart positioned on a Pulsed Local Field Fluorescence microscope and loaded with fluorescent dyes (Rhod-2 or Mag-Fluo-4 to assess cytosolic or SR Ca2+, respectively). The results indicated an initial increase in diastolic Ca2+ during early R that gradually returned to pre-ischemic levels. This increase was associated with a decrease in SR Ca2+ content that recovered within 10 min, as a mirror image of the diastolic Ca2+ profile. Additional experiments in which caffeine pulses (20 mM) were applied, confirmed that SR Ca2+ content was greatly diminished at the onset of R and gradually recovered within 10 min of R. The present findings indicate that the increase in diastolic Ca2+ that occurs upon R is due to a SR Ca2+ release and not just because of the Ca2+ entry through the reverse NCX mode, as has been previously thought. | |
| dc.description | Facultad de Ciencias Médicas | |
| dc.format | application/pdf | |
| dc.language | en | |
| dc.rights | http://creativecommons.org/licenses/by/4.0/ | |
| dc.rights | Creative Commons Attribution 4.0 International (CC BY 4.0) | |
| dc.subject | Medicina | |
| dc.subject | Calcium | |
| dc.subject | Sarcoplasmic Reticulum | |
| dc.subject | Ichemia | |
| dc.title | Reperfusion after Ichemia Causes Cytosolic Calcium Overload Due to Rapid Calcium Release from the Sarcoplasmic Reticulum | |
| dc.type | Articulo | |
| dc.type | Comunicacion | |
