Development and Long-Term Follow-Up of an Experimental Model of Myocardial Infarction in Rabbits.

Autores de INCLIVA

• 

  Patricia Genovés Martínez

  Autor

• 

  Óscar Julián Arias Mutis

  Autor

• Germán Parra Giraldo

  Autor

• 

  Luis Such Miquel

  Autor

• 

  Manuel Zarzoso Muñoz

  Autor

• Irene Del Canto Serrano

  Autor

• Carlos Soler Lopez

  Autor

• Ana Diaz Cuevas

  Autor

• Eva Blanch Torres

  Autor

• 

  Antonio M. Alberola Aguilar

  Autor

• 

  Luis Such Belenguer

  Autor

• 

  Francisco Javier Chorro Gascó

  Autor

Grupos y Plataformas de I+D+i

• Grupo de Investigación en Electrofisiología cardiaca experimental

  

  Leading Researcher

  Antonio M. Alberola Aguilar

• Grupo de Investigación en Envejecimiento Saludable

  

  Leading Researcher

  Consuelo Borras Blasco

Abstract

A chronic model of acute myocardial infarction was developed to study the mechanisms involved in adverse postinfarction ventricular remodeling. In an acute myocardial infarction (AMI), the left circumflex coronary artery of New Zealand White rabbits (n = 9) was occluded by ligature for 1 h, followed by reperfusion. A specific care protocol was applied before, during, and after the intervention, and the results were compared with those of a sham operated group (n = 7). After 5 weeks, programmed stimulation and high-resolution mapping were performed on isolated and perfused hearts using the Langendorff technique. The infarct size determined by 2,3,5-triphenyltetrazolium chloride inside of the area at risk (thioflavin-S) was then determined. The area at risk was similar in both groups (54.33% (experimental infarct group) vs. 58.59% (sham group), ns). The infarct size was 73.16% as a percentage of the risk area. The experimental infarct group had a higher inducibility of ventricular arrhythmias (100% vs. 43% in the sham group, p = 0.009). A reproducible chronic experimental model of myocardial infarction is presented in which the extent and characteristics of the lesions enable the study of the vulnerability to develop ventricular arrhythmias because of the remodeling process that occurs during cardiac tissue repair.

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)

Keywords

• myocardial infarction; ischemia; reperfusion injury; ventricular remodeling; ventricular arrhythmias; cardiac mapping; experimental surgery