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DEVELOPMENT OF AN OVINE MODEL OF MYOCARDIAL INFARCTION
Author(s) -
Rabbani Shahram,
Ahmadi Hossein,
Fayazzadeh Ehsan,
Sahebjam Mohammad,
Boroumand Mohammad A.,
Sotudeh Maryam,
Nassiri Seyed Mahdi
Publication year - 2008
Publication title -
anz journal of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.426
H-Index - 70
eISSN - 1445-2197
pISSN - 1445-1433
DOI - 10.1111/j.1445-2197.2007.04359.x
Subject(s) - medicine , hypokinesia , myocardial infarction , cardiology , infarction , coronary arteries , ejection fraction , artery , ligation , thoracotomy , surgery , heart failure
Background:  We report experimental myocardial infarction by occluding coronary arteries in ovine models. Methods:  Twelve ewes were included in the study. After the chest was opened by left lateral thoracotomy incision, the second diagonal branch of the left anterior descending coronary artery was ligated at a point approximately 40% distant from its base. Prophylactic anti‐arrhythmics were given. Animals were mechanically ventilated during surgery and stayed in intensive care unit for 24 h postoperation. Experiments were then evaluated by echocardiographic, electrocardiographic, haemodynamic, serological and morphological investigations. Echocardiographic measurements were repeated after 2 months and animals were then killed for post‐mortem cardiac examinations. Results:  All animals survived the surgical procedure. Cyanotic discoloration and hypokinesia in the cardiac tissue in an area of (30 ± 2) × (4 ± 2) mm plus ST‐segment elevations was detected immediately after vessel ligation. Moreover, there were pathological Q‐waves 2 months later. Echocardiographic evaluations showed an average of 30% relative decrease in cardiac ejection fraction. Wall motion analysis showed anteroseptal hypokinesia and akinesia in all animals 1 day and 2 months after operation, respectively. Thin‐walled infarcted areas with tissue fibrosis were evident in pathological investigations 2 months after surgery. Conclusion:  In conclusion, we developed a practical and safe method for producing myocardial infarction in large animal models.

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