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Catherine L. Stables, Michael J. Curtis, Development and characterization of a mouse in vitro model of ischaemia-induced ventricular fibrillation, Cardiovascular Research, Volume 83, Issue 2, 15 July 2009, Pages 397–404, https://doi.org/10.1093/cvr/cvp068
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Abstract
We sought to generate a mouse Langendorff model of ischaemia-induced ventricular fibrillation (VF) that does not depend on triggers such as programmed electrical stimulation.
Hearts from male Tuck Ordinary mice were perfused with Krebs solution (modified to contain low-normal K+, 3 mmol/L, and high Ca2+, 2.4 mmol/L) containing different combinations of catecholamines (epinephrine 313 nmol/L plus norepinephrine 75 nmol/L) and/or angiotensin II (100 pmol/L) designed to mimic the in vivo milieu. VF was absent during 30 min regional ischaemia (and during 10 min reperfusion) in Krebs-perfused hearts. Catecholamines unmasked ischaemia-induced VF (50%; P < 0.05) and reperfusion-induced VF (50%; P < 0.05). Co-perfusion with angiotensin II did not facilitate VF. Supraventricular pacing (600 b.p.m.) stabilized pre-ischaemic sinus rhythm and partially mimicked the VF-unmasking effect of catecholamines. Arrhythmia susceptibility was greatest with supraventricular pacing plus catecholamines (57% VF during ischaemia and 71% during reperfusion).
For the first time, regional ischaemia-induced VF was consistently evoked in a mouse Langendorff preparation, unmasked by simple periphysiological manipulation of the perfusion conditions. The model is suitable for functional genomic studies.