Abstract
Myocardial infarction (MI) remains the leading cause of death worldwide. We aimed to investigate the effect of NO deficiency on selective biochemical parameters within discreet myocardial zones after experimentally induced MI. To induce MI, the left descending coronary artery was ligated in two groups of 16-week-old WKY rats. In one group, NO production was inhibited by L-NAME (20 mg/kg/day) administration four weeks prior to ligation. Sham operations were performed on both groups as a control. Seven days after MI, we evaluated levels of nitric oxide synthase (NOS) activity, eNOS, iNOS, NFҡB/p65 and Nrf2 in ischemic, injured and non-ischemic zones of the heart. Levels of circulating TNF-α and IL-6 were evaluated in the plasma. MI led to increased NOS activity in all investigated zones of myocardium as well as circulating levels of TNF-α and IL-6. L-NAME treatment decreased NOS activity in the heart of sham operated animals. eNOS expression was increased in the injured zone and this could be a compensatory mechanism that improves the perfusion of the myocardium and cardiac dysfunction. Conversely, iNOS expression increased in the infarcted zone and may contribute to the inflammatory process and irreversible necrotic changes.
Highlights
Myocardial infarction (MI) remains the leading cause of death worldwide [1,2]
Left ventricular (LV) remodeling after MI is characterized by necrosis, excessive fibrosis, cardiomyocyte hypertrophy, inflammation and loss of capillaries, which can eventually lead to heart failure [3,4]
The reperfusion of ischemic tissue may result in additional cardiomyocyte dysfunction as a consequence of cellular enzymes released during re-oxygenation, this phenomenon is termed ischemia-reperfusion (I/R) injury [5]
Summary
Myocardial infarction (MI) remains the leading cause of death worldwide [1,2]. MI is defined as a prolonged ischemia with subsequent loss of cardiomyocytes in the infarcted area. Left ventricular (LV) remodeling after MI is characterized by necrosis, excessive fibrosis, cardiomyocyte hypertrophy, inflammation and loss of capillaries, which can eventually lead to heart failure [3,4]. Restoration of the blood supply to the ischemic myocardium is essential for limiting the damage caused by acute myocardial infarction. The reperfusion of ischemic tissue may result in additional cardiomyocyte dysfunction as a consequence of cellular enzymes released during re-oxygenation, this phenomenon is termed ischemia-reperfusion (I/R) injury [5]. The mechanism by which reperfusion contributes to additional cardiac damage is still under intense discussion. There are three major contributors to I/R injury: 1) reactive oxygen species (ROS), 2) deranged Ca2+ signaling and
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