The roles of reactive oxygen species and endogenous opioid peptides in ischemia-induced arrhythmia of isolated rat hearts

Therapeutic Effects of Xanthine Oxidase Inhibitors: Renaissance Half a Century after the Discovery of Allopurinol

“…Scheme derived from Granger et al (1981Granger et al ( , 1986 and McCord (1985). Myocardial I/R Allopurinol Improved postischemic recovery of cardiac function, but this result is attributed to an unrelated effect to XO inhibition Chambers et al (1992) Rat heart Myocardial I/R Allopurinol Increased XO activity during I/R in interstitial cells, coronary vessel endothelium, and smooth muscle cells detected by immunocytochemistry, which was reduced by allopurinol Ashraf and Samra (1993) Rat heart Myocardial I/R Allopurinol Intermittent infusion of allopurinol during global myocardial ischemia resulted in improved myocardial functional recovery and improved preservation of high-energy phosphates Sakakibara (1993) Rat heart Myocardial I/R Allopurinol Reduced the incidence and severity of reperfusion arrhythmias and increased the tissue ascorbate levels Yang et al (1995) Rat heart, right ventricular trabeculae Myocardial I/R Allopurinol, Oxypurinol Ca 2ϩ -sensitizing effect of allopurinol and oxypurinol underlying the preservation of contractility in a model of stunned myocardium Perez et al (1998) Rat heart Myocardial I/R Allopurinol Reduced accumulation of mRNA for heat shock proteins (HSP70 and HSP90) after repetitive ischemia/reperfusion Nishizawa et al (1999) Rat heart Myocardial I/R Allopurinol Allopurinol significantly inhibited myocardial xanthine oxidase activity, improved left ventricular dysfunction after ischemia, and decreased myocardial lipid peroxidation and superoxide formation…”

“…Godin and Garnett (1989) Rabbit Myocardial I/R Allopurinol Better preservation of cellular ATP levels and mitochondrial ATP generation during ischemia and prevention of the decrease in left ventricular pressure, sodium and calcium accumulation, and decreases in sarcolemmal Na ϩ ,K ϩ -stimulated and sarcoplasmic reticulum K ϩ ,Ca 2ϩ -stimulated ATPase activities Godin and Bhimji (1987) 94 (Perez et al, 1998), and effects on the antioxidant status of the cells (Qayumi et al, 1993;Yang et al, 1995)] will make the interpretation of the data difficult. Nevertheless, it is now generally accepted that XO is present in the heart (including human heart) (MacGowan et al, 1995;Berry and Hare, 2004), and substrate accumulation does occur during ischemia, which, ultimately, results in the production of free radicals during the reperfusion stage (Xia and Zweier, 1995).…”

Protective effects of the aqueous extract ofScutellaria baicalensisagainst acrolein-induced oxidative stress in cultured human umbilical vein endothelial cells

“…Protection against oxidative stress in cardiovascular disorders by using phytotherapy and western medicines has been extensively studied (Banerjee et al, 2003;Chen et al, 2009;Costa et al, 2007;Csiszar et al, 2008;He et al, 2008a;2008b;Kobayashi et al, 2002;Lakomkin et al, 2005;Liao et al, 2009;Nemoto et al, 2007;Saada et al, 2009;Vaage et al, 1997;Venardos et al, 2007;Yang et al, 1995). HUVE cells have been extensively employed to study cardiovascular diseases (Breymann et al, 2006;Chen et al, 2009;Erdbrugger et al, 1989;Morikawa et al, 2002).…”

Study of the cytotoxicity and antioxidant capacity of N/OFQ(1–13)NH2 and its structural analogues

“…The formation of superoxide and other ROS (or oxygen-derived free radicals), which may be generated by the release of endogenous opioid peptides (EOP) or by EOP/EOP receptor interactions, is suggested to be one of the major arrhythmogenic factors in ischemic hearts [42]. It has been found that ROS induce the expression of two neuropeptide genes: the opioid proenkephalin and the opioid-related proorphanin (also known as pronociceptin), suggesting a role for nociceptin in injury and stress responses of the central nervous system and in neuropathophysiological conditions [35].…”