Background &Objectives: High fat (HF) diet by affecting the oxidative stress and nitric oxide (NO) production may lead to different effects on 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 LV function after MI.
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 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: Our study indicated that HF has adverse effects on myocardium and it may increase NO production as well as oxidative stress, resulting in augmentation of infarct size.Conclusion: Our results add to our knowledge that HF diet was associated with overproduction of NO by peritoneal macrophages and ROS that lead to development of infarct size and adverse remodeling.
Cohn JN, Ferrari R, Sharpe N. Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. J. Am. Coll. Cardiol. 2000;35:569-82.
Aisagbonhi O, Rai M, Ryzhov S, Atria N, Feoktistov I, Hatzopoulos AK. Experimental myocardial infarction triggers canonical Wnt signaling and endothelial-to-mesenchymal transition. Dis. Model. Mech. 2011;4:469-83.
Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics—2011 update a report from the American Heart Association. Circulation. 2011;123:e18-e209.
Horwich TB, Fonarow GC. Glucose, obesity, metabolic syndrome, and diabetes: relevance to incidence of heart failure. J. Am. Coll. Cardiol. 2010;55:283-93.
Lindsey ML, Zamilpa R. Temporal and spatial expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases following myocardial infarction. Cardiovasc. Ther. 2012;30:31-41.
Yin H, Chao L, Chao J. Nitric oxide mediates cardiac protection of tissue kallikrein by reducing inflammation and ventricular remodeling after myocardial ischemia/reperfusion. Life. Sci. 2008;82:156-65.
Ferdinandy P, Danial H, Ambrus I, Rothery RA, Schulz R. Peroxynitrite is a major contributor to cytokine-induced myocardial contractile failure. Circ. Res. 2000;87:241-7.
Esch T, Stefano GB, Fricchione GL, Benson H. Stress-related diseases--a potential role for nitric oxide. Med. Sci. Monit. 2002;8:RA103-RA18.
Martins M, Catta-Preta M, Mandarim-de-Lacerda C, Aguila M, Brunini T, Mendes-Ribeiro A. High fat diets modulate nitric oxide biosynthesis and antioxidant defence in red blood cells from C57BL/6 mice. Arch. Biochem. Biophys. 2010;499:56-61.
Razny U, Kiec-Wilk B, Wator L, et al. Increased nitric oxide availability attenuates high fat diet metabolic alterations and gene expression associated with insulin resistance. Cardiovasc. Diabetol. 2011;10:1-14.
Lambert JM, Lopez EF, Lindsey ML. Macrophage roles following myocardial infarction. Int. J. Cardiol. 2008;130:147-58.
Snyder CM, Shroff EH, Liu J, Chandel NS. Nitric oxide induces cell death by regulating anti-apoptotic BCL-2 family members. PloS one. 2009;4:e7059.
Woods SC, Seeley RJ, Rushing PA, D’Alessio D, Tso P. A controlled high-fat diet induces an obese syndrome in rats. J. Nutr. 2003;133:1081-7.
Azizi Y, Faghihi M, Imani A, Roghani M, Nazari A. Post-infarct treatment with [Pyr1]-apelin-13 reduces myocardial damage through reduction of oxidative injury and nitric oxide enhancement in the rat model of myocardial infarction. Peptides. 2013;46:76-82.
Yaraee R, Ghazanfari T, Eghtedardoost M, Rajabi M, Naseri M. The effect of MS14 on innate and cellular immune responses in BALB/c mice. Immunopharmacol. Immunotoxicol. 2011;33:509-14.
Yassad A, Lavoinne A, Bion A, Daveau M, Husson A. Glutamine accelerates interleukin‐6 production by rat peritoneal macrophages in culture. FEBS. Lett. 1997;413:81-4.
Martins F, Campos DHS, Pagan LU, et al. High-fat diet promotes cardiac remodeling in an experimental model of obesity. Arq. Bras. Cardiol. 2015; 105:479-86.
Gaweł S, Wardas M, Niedworok E, Wardas P. Malondialdehyde (MDA) as a lipid peroxidation marker. Wiad. Lek. 2003;57:453-5.
Lorgeril M, Salen P, Accominotti M, et al. Dietary and blood antioxidants in patients with chronic heart failure. Insights into the potential importance of selenium in heart failure. Eur. J. Heart. Fail. 2001;3:661-9.
Madamanchi NR, Runge MS. Redox signaling in cardiovascular health and disease. Free. Radic. Biol. Med. 2013;61:473-501.
Kadiiska M, Gladen B, Baird D, et al. Biomarkers of oxidative stress study II: are oxidation products of lipids, proteins, and DNA markers of CCl 4 poisoning? Free. Radic. Biol. Med. 2005;38:698-710.
Lumeng CN, Bodzin JL, Saltiel AR. Obesity induces a phenotypic switch in adipose tissue macrophage polarization. J. Clin. Invest. 2007;117:175-84.
Zhao J. Interplay among nitric oxide and reactive oxygen species: a complex network determining cell survival or death. Plant. Signal. Behav. 2007;2:544-7.
Grande P, Pedersen A. Myocardial infarct size: correlation with cardiac arrhythmias and sudden death. Eur. Heart. J. 1984;5:622-7.