Author/Authors :
Aghajani، Marjan نويسنده School of Medicine,Department of physiology,Tehran University of Medical Sciences,Tehran,Iran , , Imani، Alireza نويسنده School of Medicine,Physiology Department,Tehran University of Medical Sciences,Tehran,Iran , , Faghihi، Mahdieh نويسنده School of Medicine,Department of Physiology,Tehran University of Medical Sciences,Tehran,Iran , , Vaez Mahdavi، Mohammad Reza نويسنده Medical Faculty, Traditional Medicine Clinical Trial Research Center,Department of Physiology,Shahed University,Tehran,Iran , , Mahboubi، Sarah نويسنده School of Advanced Technologies in Medicine,Department of Neuroscience,Tehran University of Medical Sciences,Tehran,Iran , , Moradi، Fatemeh نويسنده School of Medicine,Department of physiology,Tehran University of Medical Sciences,Tehran,Iran , , Kazemi Moghaddam، Ehsan نويسنده Shiraz Burn and Wound Healing Research Center, Amir-al-momenin burn hospital,Shiraz University of Medical Sciences,Shiraz,Iran ,
Abstract :
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.
Keywords :
high fat diet , Myocardial infarction , Nitric oxide , oxidative stress , Peritoneal macrophages