Cryoinfarction in rats was carried out by placing the cooled probe directly on the midway of left anterior descending coronary artery. This caused damage to the blood vessel, hindering blood flow to the distal part of the left ventricle. Gross pathology showed around 26% infarction at 24 h. Histopathology revealed death of cardiomyocytes with blood vessel congestion at the end of 24 h, inflammatory infiltrate at 48 h, fibrotic scar by 96 h and collagen deposition by 192 h. Acute myocardial infarction biomarkers such as Cardiac Troponin T, Creatine Kinase MB and NT pro BNP were shown to be elevated by 4 h. ECG showed an ST segment elevation by 96 h. This cryoinfarction model was suitable to study changes taking place during acute myocardial infarction in humans.
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Acta Histochem
October 2020
Inspired Materials & Stem-Cell Based Tissue Engineering Laboratory (IMSTEL), The University of Texas at El Paso, El Paso, TX, 79968, USA; Department of Metallurgical, Materials, and Biomedical Engineering, M201 Engineering, The University of Texas at El Paso, 500 W. University Avenue, El Paso, TX, 79968, USA; Border Biomedical Research Center, The University of Texas at El Paso, 500 W. University Avenue, El Paso, TX, 79968, USA. Electronic address:
Ligation of the left anterior descending (LAD) coronary artery has been commonly employed to induce myocardial infarction (MI) in animals; however, it is known to pose setbacks in the form of cardiac arrhythmias and unpredictable areas of necrotic damage. Cryo-infarction is an alternate method that has been adopted to create a reproducible model of a myocardial injury. In this study, Sprague-Dawley rats were subjected to thoracotomy followed by cryo-induced infarction of the heart, while the control-sham group was only subjected to thoracotomy following which the heart was collected from all animals.
View Article and Find Full Text PDFJ Physiol
September 2012
Department of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Effective management of healing and remodelling after myocardial infarction is an important problem in modern cardiology practice. We have recently shown that the level of infarct anisotropy is a critical determinant of heart function following a large anterior infarction, which suggests that therapeutic gains may be realized by controlling infarct anisotropy. However, factors regulating infarct anisotropy are not well understood.
View Article and Find Full Text PDFCryo Letters
February 2007
Department of Biotechnology, Central Leather Research Institute, Chennai, India.
Cryoinfarction in rats was carried out by placing the cooled probe directly on the midway of left anterior descending coronary artery. This caused damage to the blood vessel, hindering blood flow to the distal part of the left ventricle. Gross pathology showed around 26% infarction at 24 h.
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