Marjan Aghajani - Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran- Department of Physiology, Medical Faculty, Shahed University, Tehran, Iran
Alireza Imani - Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran- Occupational Sleep Research Center, Tehran University of Medical Sciences, Tehran, Iran
Mahdieh Faghihi - Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Mohammad Reza Vaez Mahdavi - Department of Physiology, Medical Faculty, Shahed University, Tehran, Iran- Traditional Medicine Clinical Trial Research Center, Shahed University, Tehran, Iran
Sarah Mahboubi - Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
Fatemeh Moradi - Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Background: High fat (HF) diet by affecting the oxidative stress and nitric oxide (NO) production may lead to different effects on the function of the heart after myocardial infarction (MI). In the present study, we aimed to address the hypothesis that high release of NO by activated macrophages affects left ventricular function after myocardial infarction.Materials and Methods: The animals were randomly divided into four groups comprising each of 10 rats: 1) Sham; 2) MI; 3) Sham+ HF diet; 4) MI+ HF diet. Animals fed with HF diet 30 days before sham and MI surgery. MI was induced by permanent ligation of the left anterior descending coronary artery (LAD). Nitric oxide (NO) production of peritoneal macrophages, the concentrations of MDA in the heart and the infarct size were measured.Results: HF group had adverse effects on myocardium; also, HF group had increased level of NO production as well as oxidative stress, associated with augmentation of infarct size.Conclusion: Our results add to our knowledge that HF diet was associated with overproduction of NO by peritoneal macrophages and reactive oxygen species that lead to the development of infarct size and adverse remodeling.

High fat diet, myocardial infarction, Nitric oxide, oxidative stress, peritoneal macrophages