oxidase/infarction

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Chronic xanthine oxidase inhibition following myocardial infarction in rabbits: effects of early versus delayed treatment.

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Xanthine oxidase (XO) expression is increased in the failing heart, and animal studies in rodents and dogs showed that XO inhibition with allopurinol can improve left ventricular (LV) function and myocardial oxygen efficiency in the failing heart. The purpose of this study was to determine whether

Xanthine oxidase as a marker of myocardial infarction.

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In the present communication, we report remarkably elevated levels of xanthine oxidase activity in the blood of the patients with myocardial infarction when compared to age and sex matched healthy persons. Highly significant increase of malondialdehyde, serving as an index of lipid peroxidation and

Immunohistochemical detection of differentially localized up-regulation of lysyl oxidase and down-regulation of matrix metalloproteinase-1 in rhesus monkey model of chronic myocardial infarction.

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Myocardial remodeling after ischemic infarction is characterized by collagen accumulation leading to replacement and interstitial fibrosis. Type I and III collagens are predominant components in cardiac fibrosis. Lysyl oxidase (LOX) facilitates the cross-linking of type I and III fibrils, resulting

Pharmacological inhibition of the mitochondrial NADPH oxidase 4/PKCα/Gal-3 pathway reduces left ventricular fibrosis following myocardial infarction.

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Although the initial reparative fibrosis after myocardial infarction (MI) is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental. Although metformin prevents adverse cardiac remodeling, as well as

Critical role for white blood cell NAD(P)H oxidase-mediated plasminogen activator inhibitor-1 oxidation and ventricular rupture following acute myocardial infarction.

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Plasminogen activator inhibitor-1 (PAI-1) is an oxidant-sensitive protease inhibitor that is inactivated by oxidation and has a critical role in ventricular remodeling post myocardial infarction (MI). PAI-1 knockout (KO) mice die within 7days of myocardial infarction post MI due to increased plasmin

Does verapamil limit myocardial infarct size in a heart deficient in xanthine oxidase?

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1. The delay of ischaemic myocardial necrosis by verapamil has been reported in the dog heart, which contains a high level of xanthine oxidase, a potential source of cytotoxic free radicals. To test whether the retardation of ischaemic myocyte death by verapamil is not an isolated phenomenon in the

Xanthine Oxidase Activation Modulates the Endothelial (Vascular) Dysfunction Related to HgCl2 Exposure Plus Myocardial Infarction in Rats.

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Heavy metal exposure is associated with cardiovascular diseases such as myocardial infarction (MI). Vascular dysfunction is related to both the causes and the consequences of MI. We investigated whether chronic exposure to low doses of mercury chloride (HgCl2) worsens MI-induced endothelial

Functional effects of NAD(P)H oxidase p22(phox) C242T mutation in human leukocytes and association with thrombotic cerebral infarction.

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BACKGROUND Previous study showed that polymorphism of the NAD(P)H oxidase p22(phox) gene is associated with atherosclerosis, although others could not confirm such association. We investigated the association between p22(phox) C242T polymorphism and thrombotic cerebral infarction and the role of

Inhibition of NADPH oxidase reduces myocardial oxidative stress and apoptosis and improves cardiac function in heart failure after myocardial infarction.

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Increases in NADPH oxidase activity, oxidative stress, and myocyte apoptosis coexist in failing hearts. In cardiac myocytes in vitro inhibition of NADPH oxidase reduces apoptosis. In this study, we tested the hypothesis that NADPH oxidase inhibition reduces myocyte apoptosis and improves cardiac

Ectopic ventricular rhythms and myocardial infarction in the domestic pig and their response to nialamide, a monoamine oxidase inhibitor.

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The development in Indian domestic pigs of ectopic ventricular rhythms and a low-frequency tachycardia after the two-stage ligature of the anterior descending branch of the left coronary artery is described. When the ligature was tied 26+/-3 mm from the left auricular margin, the change in rhythm

Left ventricular remodeling after myocardial infarction in mice with targeted deletion of the NADPH oxidase subunit gp91PHOX.

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BACKGROUND Oxidative stress is involved in progression of left ventricular hypertrophy and heart failure. Since NADPH oxidases are a major source of reactive oxygen species in the heart, we studied left ventricular remodeling after myocardial infarction in mice with targeted deletion of the NADPH

Histochemical studies of monoamine oxidase in experimental myocardial infarctions.

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Sequential histochemical studies were conducted to determine the level of monoamine oxidase (MAO) activity in the infarcted tissue of the experimental myocardial infarction in dog. MAO activity was not found in the normal heart muscle, but the activities were present in the wall of the coronary

The xanthine oxidase inhibitor oxypurinol does not limit infarct size in a canine model of 40 minutes of ischemia with reperfusion.

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Free radicals such as superoxide (.O2-) produced by xanthine oxidase might cause cell death during reperfusion after myocardial ischemia. The effect of the xanthine oxidase inhibitor allopurinol on infarct size in ischemia-reperfusion models has been variable, possibly because of differences in

Nitrite confers protection against myocardial infarction: role of xanthine oxidoreductase, NADPH oxidase and K(ATP) channels.

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Reduction of nitrite to nitric oxide during ischemia protects the heart against injury from ischemia/reperfusion. However the optimal dose of nitrite and the mechanisms underlying nitrite-induced cardioprotection are not known. We determined the ability of nitrite and nitrate to confer protection

Relationship between NADPH oxidase p22phox C242T, PARP-1 Val762Ala polymorphisms, angiographically verified coronary artery disease and myocardial infarction in South Indian patients with type 2 diabetes mellitus.

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BACKGROUND There has been compelling evidence for the role of oxidative stress in the pathogenesis of cardiovascular complications in type 2 diabetes mellitus (T2DM). We analyzed the association of C242T and Val762Ala polymorphisms of NADPH oxidase p22phox and poly (ADP-ribose) polymerase-1 (PARP-1)

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