Allopurinol Improves Cardiac Dysfunction After Ischemia-Reperfusion via Reduction of Oxidative Stress in Isolated Perfused Rat Hearts

Kinugasa, Yoshiharu; Oginö, Kazuhíde; Furuse, Yoshiyuki; Shiomi, Tetsuya; Tsutsui, Hiroyuki; Yamamoto, Tetsuya; Igawa, Osamu; Hisatome, Ichiro; Shigemasa, Chiaki

doi:10.1253/circj.67.781

Cited by 70 publications

(71 citation statements)

References 38 publications

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“…1 Oxidative stress induced by superoxide generated via the xanthine oxidase system and infiltrating inflammatory cells is the major proposed mechanism of MIR progression. [2][3][4][5] We have reported that reactive oxygen species (ROS) influence the opening of the mitochondrial permeability transition pore in myocardial cells, which led to progression of myocardial infarction (MI) in a rat MIR model. 6 Moreover, total nitric oxide (NO) synthesis in the reperfused heart was increased in previous investigations.…”

mentioning

confidence: 99%

Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia Reperfusion

Yamamoto

Maeda

Hirose

et al. 2008

Circ J

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lthough therapeutic intervention or coronary artery bypass grafting can recover coronary blood flow, myocardial damage after blood flow reperfusion, namely myocardial ischemia reperfusion (MIR) injury, remains to be resolved. Among the factors affecting MIR, oxidative stress might play an important role in both the myocardial injury and the cardiac events after reperfusion therapy. 1 Oxidative stress induced by superoxide generated via the xanthine oxidase system and infiltrating inflammatory cells is the major proposed mechanism of MIR progression. [2][3][4][5] We have reported that reactive oxygen species (ROS) influence the opening of the mitochondrial permeability transition pore in myocardial cells, which led to progression of myocardial infarction (MI) in a rat MIR model. 6 Moreover, total nitric oxide (NO) synthesis in the reperfused heart was increased in previous investigations. 7-9 Physiological concentrations of NO produced from endothelial NO synthase (eNOS) or NO donors exert significant cardioprotective effects, whereas the reaction between NO and ROS produces peroxynitrite and results in oxidative and nitrative tissue injury. [7][8][9][10][11][12][13] Evidence from several model systems supports the notion that NO radicals cause myocardial damage in MIR, 7,8,[12][13][14][15] whereas a small amount of NO exerts a cytoprotective effect in the reperfused heart. 11,12,16,17 The dynamics of oxidative stress up to 48 h after MIR remain unclear because of the difficulties associated with monitoring oxidation in vivo. This period is considered critical in both cardiac surgery and therapeutic intervention, so more sensitive and reliable markers of in vivo oxidative stress are required.Bilirubin is an intrinsic antioxidant that quenches radicals under several inflammatory conditions. 18-21 Its synthesis is regulated by the rate-limiting enzyme, heme oxygenase-1 (HO-1), which is rapidly induced by oxidative stress and inflammatory reactions caused by factors such as cytokines, ischemia and NO. [22][23][24][25][26][27][28][29] Bilirubin generates several hydrophilic metabolites called biopyrrins upon oxidation and these can be detected using the anti-bilirubin monoclonal antibody 24G7. 30,31 Biopyrrins are immediately excreted in urine because of their hydrophilic properties and thus can reflect the severity of oxidative stress. 25,[32][33][34][35][36][37][38] Biopyrrin synthesis reflects NO radicals, 25 so urinary biopyrrin levels can indicate ongoing changes in oxidative stress in vivo and thus function as a marker of oxidative stress.The time course of urinary and tissue biopyrrin levels in rat models of cardiac transplantation and hepatic ischemia reperfusion has been investigated. 25,32 A cardiac transplantation study showed that levels of urinary biopyrrins become more rapidly and sensitively elevated than either urinary 8-hydroxy-2'-deoxyguanosine or serum troponin-T during Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia ReperfusionMasaki Yamamoto, MD; Hironori Maeda, MD; Nobuyuki...

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confidence: 99%

Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia Reperfusion

Yamamoto

Maeda

Hirose

et al. 2008

Circ J

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“…However, previous studies have shown that antioxidant drugs improve post-ischemic cardiac dysfunction in isolated hearts. 22,23 Therefore, because nicorandil has been reported to have many beneficial effects, such as opening the mitochondrial KATP channels, 4,5 inhibiting apoptosis, 24 inhibiting platelet aggregation, 25 direct preservation of mitochondrial function, 26 and coronary capillary architecture and volume, 27 besides free radical scavenging effects, it is still difficult to say whether the decrease in 2,3-DHBA concentration is the main cause of the attenuation of ischemia -reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Nicorandil Improves Post-Ischemic Myocardial Dysfunction in Association With Opening the Mitochondrial K<sub>ATP</sub> Channels and Decreasing Hydroxyl Radicals in Isolated Rat Hearts

Minatoguchi

Arai

et al. 2006

Circ J

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“…Next, they were subjected to a 30-min no flow global ischemia, followed by 60 min of reperfusion. 16 The successful induction of ischemia was determined by ST elevation on the electrocardiogram. Heart rate and perfusion pressure were constantly monitored.…”

Section: Isolation and Preparation Of The Heartmentioning

confidence: 99%

Gallic Acid and Cyclosporine Mixture and their Effects on Cardiac Dysfunction Induced by Ischemia/Reperfusion and eNOS/iNOS Expression

Badavi

Sadeghi

Dianat

et al. 2017

International Journal of Cardiovascular Sciences

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Allopurinol Improves Cardiac Dysfunction After Ischemia-Reperfusion via Reduction of Oxidative Stress in Isolated Perfused Rat Hearts

Cited by 70 publications

References 38 publications

Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia Reperfusion

Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia Reperfusion

Nicorandil Improves Post-Ischemic Myocardial Dysfunction in Association With Opening the Mitochondrial K<sub>ATP</sub> Channels and Decreasing Hydroxyl Radicals in Isolated Rat Hearts

Gallic Acid and Cyclosporine Mixture and their Effects on Cardiac Dysfunction Induced by Ischemia/Reperfusion and eNOS/iNOS Expression

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