Ischemic Preconditioning Attenuates Postischemic Leukocyte - Endothelial Cell Interactions Role of Nitric Oxide and Protein Kinase C

Huang, Shiang‐Suo; Wei, Fu‐Chan; Hung, Li-Man

doi:10.1253/circj.70.1070

Cited by 44 publications

(23 citation statements)

References 46 publications

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“…[8][9][10][11][12][13] Huang et al showed that the inhibition of iNOS activity blocks the increase in the number of leukocytes that synthesize ROS after MIR. 40 In the present study, we demonstrated that the urinary and tissue biopyrrins concentrations were obviously reduced with nonselective suppression of NOS expression. Moreover, the infarct size and myocardial dysfunction were reduced with L-NMMA administration.…”

Section: Discussionsupporting

confidence: 57%

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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Section: Discussionsupporting

confidence: 57%

Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia Reperfusion

Yamamoto

Maeda

Hirose

et al. 2008

Circ J

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“…5,22 Furthermore, ischemia-reperfusion induces a marked increase of TNF-that in turn increases pulmonary endothelial permeability. 23,24 In the present study, TNF-increased after reperfusion and decreased with IMP administration, resulting in changes in MPO activity, neutrophil infiltration and SpO2. Taken together, it is possible that skeletal muscle ischemia-reperfusion induces TNF-production, leading to lung inflammation, and that IMP administration ameliorates the lung injury via the suppression of TNF-.…”

Section: Discussionsupporting

confidence: 52%

Remote Reperfusion Lung Injury is Associated With AMP Deaminase 3 Activation and Attenuated by Inosine Monophosphate

Oginö

Hoshikawa

et al. 2007

Circ J

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“…27 Huang et al reported that NOS also has a protective effect against myocardial injury during ischemiareperfusion. 28 However, no data have been published to document the possible effects of NOS inhibition on the direct control of PVA-independent MV • O2 or MV • O2 for E-C coupling. Further studies are therefore warranted to examine the effect of cardiac NOS inhibition on PVA-independent MV…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Endogenous Nitric Oxide Synthase Augments Contractile Response to Adenylyl Cyclase Stimulation Without Altering Mechanical Efficiency in Patients With Idiopathic Dilated Cardiomyopathy

Ohta

Shinke

Hata

et al. 2007

Circ J

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itric oxide (NO) is an important regulator of cardiac function. 1,2 In patients with congestive heart failure (CHF) the concentrations of NO and tumor necrosis factor-increase in proportion to the severity of heart failure. 3,4 Previous studies have shown that inhibition of cardiac NO synthase (NOS) augments the positive inotropic response to -adrenergic receptor stimulation in human heart failure, suggesting that increased activity of myocardial NOS and NO attenuates -adrenergic responsiveness. [5][6][7] In patients with severe CHF, the increase in intracellular cyclic AMP and myocardial contractility in response toadrenergic receptor stimulation is reduced, 5 which reflects cardiac desensitization to -receptor agonists, 8 partly modulated by the increased production of NO in the myocardium. 5 Previous studies have shown that forskolin produces beneficial cardiac effects by directly stimulating adenylyl cyclase in the failed human heart, especially in those with a relative insensitivity to -adrenergic receptor stimulation. 9 Colforsin daropate (NKH477; 6-(3-dimethyl-aminopropionyl) forskolin hydrochloride) is a new water-soluble forskolin derivative, which experimental studies have shown to be able to generate positive inotropic and vasodilatory actions. 10,11 Furthermore, we previously reported that NKH477 might be a superior alternative to dobutamine for mechanical energy transduction in patients with left ventricular (LV) systolic dysfunction. 12 It remains to be clarified how NO modulates -adrenergic post-receptor signaling, such as adenylyl cyclase stimulation in the failing human heart. The objective of this study was to address the role of NO by evaluating the effects of cardiac NOS inhibition on LV hemodynamics and mechanoenergetics in response to adenylyl cyclase stimulation with colforsin daropate in patients with idiopathic cardiomyopathy (IDC). Methods Study SubjectsWe examined 13 patients (10 men, 3 women, mean age 56±13 years) who were undergoing diagnostic cardiac catheterization for the evaluation of heart failure on their first admission to hospital. All patients showed normal sinus rhythm and were diagnosed as IDC by the absence of coronary artery disease or other known causes of dilated cardiomyopathy. The patients were in New York Heart Association functional class II (n=8) or class III (n=5) with a LV ejection fraction (LVEF) of less than 40%. None of Background Increased nitric oxide (NO) in the failing heart attenuates the myocardial contractile response to -adrenergic receptor stimulation. However, the physiological effects of NO on the -adrenergic post-receptor signaling system are unknown. The objective of the present study was to examine the effects of cardiac NO synthase (NOS) inhibition on left ventricular (LV) hemodynamics and mechanoenergetics in response to adenylyl cyclase stimulation in human heart failure. Methods and ResultsThe study group comprised 13 patients with heart failure because of idiopathic cardiomyopathy (IDC). Emax was examined as an index of LV contractility, LV...

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Ischemic Preconditioning Attenuates Postischemic Leukocyte - Endothelial Cell Interactions Role of Nitric Oxide and Protein Kinase C

Cited by 44 publications

References 46 publications

Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia Reperfusion

Biphasic Elevation of Bilirubin Oxidation During Myocardial Ischemia Reperfusion

Remote Reperfusion Lung Injury is Associated With AMP Deaminase 3 Activation and Attenuated by Inosine Monophosphate

Inhibition of Endogenous Nitric Oxide Synthase Augments Contractile Response to Adenylyl Cyclase Stimulation Without Altering Mechanical Efficiency in Patients With Idiopathic Dilated Cardiomyopathy

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