Oxidative stress and antioxidative defense parameters early after reperfusion therapy for acute myocardial infarction

Abstract

Reperfusion of ischemic myocardium evokes rapid release of free radicals in experimental models. The aim of the study was to investigate the oxidative stress and antioxidative defense during first minutes after reopening of the infarct related artery in patients treated for acute myocardial infarction. The study group consisted of 15 patients with first ST elevation myocardial infarction (STEMI) due to left anterior descending artery occlusion. The control group included ten patients with stable ischemic heart disease (IHD). Blood samples from coronary sinus were drawn before, immediately after and about 15 min after angioplasty. Activity of superoxide dysmutase (SOD), concentration of glutathione as well as the concentrations of lipid peroxides, malodialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE) were measured. There was significantly higher concentration of MDA and HNE and higher SOD activity in STEMI patients before the reperfusion, as compared to the stable IHD group. After the reperfusion concentration of HNE in erythrocytes from STEMI patients was higher than in IHD group. At the same time the activity of SOD significantly decreased in patients with impaired tissue perfusion (myocardial blush grade <2). In conclusion, there is a slightly higher concentration of oxidative stress parameters in patients with STEMI. Diminished antioxidative defense after reperfusion is associated with impaired myocardial perfusion.

Hydroxyalkenals and oxidized phospholipids modulation of endothelial cytoskeleton, focal adhesion and adherens junction proteins in regulating endothelial barrier function

“…However, under conditions of oxidative stress, 4-HNE accumulates in tissues up to concentration of 10 μM to 5 mM (Esterbauer et al, 1991). Post-hypoxic re-oxygenation condition or post-ischemic organ reperfusion results in enhanced 4-HNE level in different tissues and organs such as liver (hepatocytes), heart and small intestine (Compton et al, 1998; Eaton et al, 1999; Gutierrez et al, 2006; Hamilton et al, 1998; Kaminski et al, 2008; Mertsch et al, 2001; Nakamura et al, 2009; Rahman et al, 2002; Renner et al, 2005). 4-HNE accumulation is regulated by multiple pathways involved in its detoxification and mediated (Fig.…”

“…There is evidence in the literature that show an association between increased levels of 4-HNE and other lipid peroxidation products and development of oxidative stress-related human disorders (Berliner and Gharavi, 2008; Bochkov et al, 2010; Eaton et al, 1999; Hamilton et al, 1998; Herbst et al, 1999; Kaminski et al, 2008; Mertsch et al, 2001; Nakamura et al, 2009; Rahman et al, 2002; Renner et al, 2005; Uchida et al, 1999; Yang et al, 2004); however, it is unclear if hydroxyalkenals have a direct role in the pathophysiology or are a consequence. Moreover, hydroxyalkenals and Ox-PLs play a role as intracellular signaling molecules altering cellular responses to stress and toxicity, modulate cellular DNA, RNA, and protein synthesis, cell growth, and differentiation, and apoptosis (Bochkov et al, 2010; Parola et al, 1999; Poli et al, 2008; Uchida, 2003).…”

“…Increased levels of 4-HNE invoke a wide range of biological activities and activation of stress signaling pathways. Several in vivo and in vitro studies have demonstrated that 4-HNE is a key player in cardiovascular and lung disorders (Kaminski et al, 2008; Negre-Salvayre et al, 2010; Parola et al, 1999; Poli et al, 2008; Uchida, 2003; Uchida et al, 1999; Yang et al, 2003b). The formation and accumulation 4-HNE in tissues have been shown under different pathophysiological conditions.…”

“…The formation and accumulation 4-HNE in tissues have been shown under different pathophysiological conditions. Enhanced levels of 4-HNE-modified proteins have been described in ischemic rat hearts or airway and alveolar epithelial cells, and in endothelial cells of subjects with chronic obstructive pulmonary disease (COPD) (Chaudhary et al, 2010; Compton et al, 1998; Eaton et al, 1999; Gutierrez et al, 2006; Herbst et al, 1999; Kaminski et al, 2008; Mertsch et al, 2001; Rahman et al, 2002; Uchida et al, 1999). In human, ozone exposure causes formation of protein adducts, induction of stress proteins and apoptosis in airway and lung cells (Hamilton et al, 1998).…”

The effect of antioxidant enzyme levels and exercise on syndrome X and coronary slow flow phenomenon: an observational study

“…It has been thought that, slow coronary flow and syndrome X are part of this process (2)(3)(4)(5)(6)(7)(8)(9). The relation between oxidant enzyme level and coronary artery disease has been revealed by previous studies (10)(11)(12)(13).…”