Matches in UGent Biblio for { <https://biblio.ugent.be/publication/3116576#aggregation> ?p ?o. }
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- aggregation classification "A1".
- aggregation creator B511709.
- aggregation creator B511710.
- aggregation creator B511711.
- aggregation creator B511712.
- aggregation creator B511713.
- aggregation creator person.
- aggregation creator person.
- aggregation date "2013".
- aggregation format "application/pdf".
- aggregation hasFormat 3116576.bibtex.
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- aggregation isPartOf urn:issn:0008-6363.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Prolongation of minimal action potential duration in sustained fibrillation decreases complexity by transient destabilization".
- aggregation abstract "Sustained ventricular fibrillation (VF) is maintained by multiple stable rotors. Destabilization of sustained VF could be beneficial by affecting VF complexity (defined by the number of rotors). However, underlying mechanisms affecting VF stability are poorly understood. Therefore, the aim of this study was to correlate changes in arrhythmia complexity with changes in specific electrophysiological parameters, allowing a search for novel factors and underlying mechanisms affecting stability of sustained VF. Neonatal rat ventricular cardiomyocyte monolayers and Langendorff-perfused adult rat hearts were exposed to increasing dosages of the gap junctional uncoupler 2-aminoethoxydiphenyl borate (2-APB) to induce arrhythmias. Ion channel blockers/openers were added to study effects on VF stability. Electrophysiological parameters were assessed by optical mapping and patch-clamp techniques. Arrhythmia complexity in cardiomyocyte cultures increased with increasing dosages of 2-APB (n 38), leading to sustained VF: 0.0 0.1 phase singularities/cm(2) in controls vs. 0.0 0.1, 1.0 0.9, 3.3 3.2, 11.0 10.1, and 54.3 21.7 in 5, 10, 15, 20, and 25 mol/L 2-APB, respectively. Arrhythmia complexity inversely correlated with wavelength. Lengthening of wavelength during fibrillation could only be induced by agents (BaCl2/BayK8644) increasing the action potential duration (APD) at maximal activation frequencies (minimal APD); 123 32/117 24 of control. Minimal APD prolongation led to transient VF destabilization, shown by critical wavefront collision leading to rotor termination, followed by significant decreases in VF complexity and activation frequency (52/37). These key findings were reproduced ex vivo in rat hearts (n 6 per group). These results show that stability of sustained fibrillation is regulated by minimal APD. Minimal APD prolongation leads to transient destabilization of fibrillation, ultimately decreasing VF complexity, thereby providing novel insights into anti-fibrillatory mechanisms.".
- aggregation authorList BK858107.
- aggregation endPage "170".
- aggregation issue "1".
- aggregation startPage "161".
- aggregation volume "97".
- aggregation aggregates 3128121.
- aggregation isDescribedBy 3116576.
- aggregation similarTo cvs288.
- aggregation similarTo LU-3116576.