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10.1161/CIRCRESAHA.114.302505 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.114.302505 C4000583!4000583 !24568740     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24568740 &cmd=llinks): Failed to open stream: HTTP request failed! 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Optical mapping of sarcoplasmic reticulum Ca2+ in the intact heart: ryanodine receptor refractoriness during alternans and fibrillation |pdf=|usr=}}{{24568740 }} gab.com Text Optical mapping of sarcoplasmic reticulum Ca2+ in the intact heart: ryanodine receptor refractoriness during alternans and fibrillation JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=24568740 #FOAvip RATIONALE: Sarcoplasmic reticulum (SR) Ca(2+) cycling is key to normal excitation-contraction coupling but may also contribute to pathological cardiac alternans and arrhythmia. OBJECTIVE: To measure intra-SR free [Ca(2+)] ([Ca(2+)]SR) changes in intact hearts during alternans and ventricular fibrillation (VF). METHODS AND RESULTS: Simultaneous optical mapping of Vm (with RH237) and [Ca(2+)]SR (with Fluo-5N AM) was performed in Langendorff-perfused rabbit hearts. Alternans and VF were induced by rapid pacing. SR Ca(2+) and action potential duration (APD) alternans occurred in-phase, but SR Ca(2+) alternans emerged first as cycle length was progressively reduced (217±10 versus 190±13 ms; P<0.05). Ryanodine receptor (RyR) refractoriness played a key role in the onset of SR Ca(2+) alternans, with SR Ca(2+) release alternans routinely occurring without changes in diastolic [Ca(2+)]SR. Sensitizing RyR with caffeine (200 ?mol/L) significantly reduced the pacing threshold for both SR Ca(2+) and APD alternans (188±15 and 173±12 ms; P<0.05 versus baseline). Caffeine also reduced the magnitude of spatially discordant SR Ca(2+) alternans, but not APD alternans, the pacing threshold for discordance, or threshold for VF. During VF, [Ca(2+)]SR was high, but RyR remained nearly continuously refractory, resulting in minimal SR Ca(2+) release throughout VF. CONCLUSIONS: In intact hearts, RyR refractoriness initiates SR Ca(2+) release alternans that can be amplified by diastolic [Ca(2+)]SR alternans and lead to APD alternans. Sensitizing RyR suppresses spatially concordant but not discordant SR Ca(2+) and APD alternans. Despite increased [Ca(2+)]SR during VF, SR Ca(2+) release was nearly continuously refractory. This novel method provides insight into SR Ca(2+) handling during cardiac alternans and arrhythmia. Twit Text FOAVip Optical mapping of sarcoplasmic reticulum Ca2+ in the intact heart: ryanodine receptor refractoriness during alternans and fibrillation ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=24568740 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24568740 #FOAvip English Wikipedia <ref>{{Cite pmid|24568740 }}</ref> Optical mapping of sarcoplasmic reticulum Ca2+ in the intact heart: ryanodine receptor refractoriness during alternans and fibrillation #MMPMID24568740 Wang L ; Myles RC ; De Jesus NM ; Ohlendorf AK ; Bers DM ; Ripplinger CM Circ Res 2014[Apr]; 114 (9 ): 1410-21 PMID24568740 show ga RATIONALE: Sarcoplasmic reticulum (SR) Ca(2+) cycling is key to normal excitation-contraction coupling but may also contribute to pathological cardiac alternans and arrhythmia. OBJECTIVE: To measure intra-SR free [Ca(2+)] ([Ca(2+)]SR) changes in intact hearts during alternans and ventricular fibrillation (VF). METHODS AND RESULTS: Simultaneous optical mapping of Vm (with RH237) and [Ca(2+)]SR (with Fluo-5N AM) was performed in Langendorff-perfused rabbit hearts. Alternans and VF were induced by rapid pacing. SR Ca(2+) and action potential duration (APD) alternans occurred in-phase, but SR Ca(2+) alternans emerged first as cycle length was progressively reduced (217±10 versus 190±13 ms; P<0.05). Ryanodine receptor (RyR) refractoriness played a key role in the onset of SR Ca(2+) alternans, with SR Ca(2+) release alternans routinely occurring without changes in diastolic [Ca(2+)]SR. Sensitizing RyR with caffeine (200 ?mol/L) significantly reduced the pacing threshold for both SR Ca(2+) and APD alternans (188±15 and 173±12 ms; P<0.05 versus baseline). Caffeine also reduced the magnitude of spatially discordant SR Ca(2+) alternans, but not APD alternans, the pacing threshold for discordance, or threshold for VF. During VF, [Ca(2+)]SR was high, but RyR remained nearly continuously refractory, resulting in minimal SR Ca(2+) release throughout VF. CONCLUSIONS: In intact hearts, RyR refractoriness initiates SR Ca(2+) release alternans that can be amplified by diastolic [Ca(2+)]SR alternans and lead to APD alternans. Sensitizing RyR suppresses spatially concordant but not discordant SR Ca(2+) and APD alternans. Despite increased [Ca(2+)]SR during VF, SR Ca(2+) release was nearly continuously refractory. This novel method provides insight into SR Ca(2+) handling during cardiac alternans and arrhythmia. |*Calcium Signaling/drug effects [MESH] |*Refractory Period, Electrophysiological [MESH] |*Voltage-Sensitive Dye Imaging [MESH] |Action Potentials [MESH] |Adrenergic beta-Agonists/pharmacology [MESH] |Animals [MESH] |Caffeine/pharmacology [MESH] |Calcium/*metabolism [MESH] |Cardiac Pacing, Artificial [MESH] |Excitation Contraction Coupling [MESH] |In Vitro Techniques [MESH] |Isoproterenol/pharmacology [MESH] |Myocytes, Cardiac/drug effects/*metabolism [MESH] |Perfusion [MESH] |Rabbits [MESH] |Receptors, Adrenergic, beta/drug effects/metabolism [MESH] |Ryanodine Receptor Calcium Release Channel/drug effects/*metabolism [MESH] |Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism [MESH] |Sarcoplasmic Reticulum/drug effects/*metabolism [MESH] |Time Factors [MESH]Optical mapping of sarcoplasmic reticulum Ca2+ in the intact heart: ry(epmc).pdf DeepDyve Pubget Overpricing