info:eu-repo/semantics/article
Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
Fecha
2010-03Registro en:
Valverde, Carlos Alfredo; Kornyeyev, Dmytro; Ferreiro, Marcela; Petrosky, Azadé D.; Mattiazzi, Ramona Alicia; et al.; Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion; Oxford University Press; Cardiovascular Research; 85; 4; 3-2010; 671-680
0008-6363
CONICET Digital
CONICET
Autor
Valverde, Carlos Alfredo
Kornyeyev, Dmytro
Ferreiro, Marcela
Petrosky, Azadé D.
Mattiazzi, Ramona Alicia
Escobar, Ariel Luis Manuel
Resumen
AimsMyocardial stunning is a contractile dysfunction that occurs after a brief ischaemic insult. Substantial evidence supports that this dysfunction is triggered by Ca2+ overload during reperfusion. The aim of the present manuscript is to define the origin of this Ca2+ increase in the intact heart.Methods and resultsTo address this issue, Langendorff-perfused mouse hearts positioned on a pulsed local field fluorescence microscope and loaded with fluorescent dyes Rhod-2, Mag-fluo-4, and Di-8-ANEPPS, to assess cytosolic Ca2+, sarcoplasmic reticulum (SR) Ca2+, and transmembrane action potentials (AP), respectively, in the epicardial layer of the hearts, were submitted to 12 min of global ischaemia followed by reperfusion. Ischaemia increased cytosolic Ca2+ in association with a decrease in intracellular Ca2+ transients and a depression of Ca2+ transient kinetics, i.e. the rise time and decay time constant of Ca2+ transients were significantly prolonged. Reperfusion produced a transient increase in cytosolic Ca2+ (Ca2+ bump), which was temporally associated with a decrease in SR-Ca2+ content, as a mirror-like image. Caffeine pulses (20 mM) confirmed that SR-Ca2+ content was greatly diminished at the onset of reflow. The SR-Ca2+ decrease was associated with a decrease in Ca2+ transient amplitude and a shortening of AP duration mainly due to a decrease in phase 2.ConclusionTo the best of our knowledge, this is the first study in which SR-Ca2+ transients are recorded in the intact heart, revealing a previously unknown participation of SR on cytosolic Ca2+ overload upon reperfusion in the intact beating heart. Additionally, the associated shortening of phase 2 of the AP may provide a clue to explain early reperfusion arrhythmias.