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Cardiovascular Research Advance Access [Accepted Manuscript] published online on February 19, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp068
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Development and characterization of a mouse in vitro model of ischemia-induced ventricular fibrillation

Catherine L. Stables and Michael J. Curtis*

King's College London, Cardiovascular Division, St Thomas' Hospital, London, SE1 7EH, UK

* Author for correspondence: Tel: +44 207 1881095 Fax: +44 207 1880970 Email: michael.curtis{at}kcl.ac.uk

Aims: We sought to generate a mouse Langendorff model of ischemia-induced ventricular fibrillation (VF) that does not depend on triggers such as programmed electrical stimulation

Methods: 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.

Results: VF was absent during 30 min regional ischemia (and during 10 min reperfusion) in Krebs-perfused hearts. Catecholamines unmasked ischemia-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 beats/min) 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 ischemia and 71% during reperfusion).

Conclusions: For the first time, regional ischemia-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.

KEYWORDS antiarrhythmic agents; ischemia; mouse models; sudden death; ventricular arrhythmias

Time for primary review: 21 days


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