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Страница 1 от 587 резултата
Temporal effects of catalase overexpression on healing after myocardial infarction.
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BACKGROUND
Reactive oxygen species, such as hydrogen peroxide (H(2)O(2)), contribute to progression of dysfunction after myocardial infarction (MI). However, chronic overexpression studies do not agree with acute protein delivery studies. The purpose of the present study was to assess the temporal
Over-expression of catalase in myeloid cells confers acute protection following myocardial infarction.
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Cardiovascular disease is the leading cause of death in the United States and new treatment options are greatly needed. Oxidative stress is increased following myocardial infarction and levels of antioxidants decrease, causing imbalance that leads to dysfunction. Therapy involving catalase, the
Superoxide dismutase and catalase reduce infarct size in a porcine myocardial occlusion-reperfusion model.
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We investigated if superoxide dismutase and catalase could reduce myocardial infarct size in an open chest occlusion-reperfusion model. Thirty pigs were used for the experiment. The left anterior descending artery was ligated for 60 min followed by a 5 h reperfusion period. After randomisation and
Beneficial effects of coronary venous retroinfusion of superoxide dismutase and catalase on reperfusion arrhythmias, myocardial function, and infarct size in dogs.
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The efficacy of coronary venous retroinfusion of superoxide dismutase and catalase was studied in anesthetized closed chest dogs with 90-min left anterior descending coronary artery (LAD) occlusion followed by 3-h reperfusion. In group A, superoxide dismutase (2.5 mg/kg) and catalase (2.5 mg/kg)
Hyperbaric oxygenation pretreatment induces catalase and reduces infarct size in ischemic rat myocardium.
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Ischemia-reperfusion injury is a major complication occurring in heart stroke, cardiopulmonary bypass surgeries, and heart transplantation. Reactive oxygen species generated during the reperfusion phase overwhelm the scavenging capacities of antioxidant enzymes, and result in oxidative damage to the
Catalase inhibition with 3-amino-1,2,4-triazole does not abolish infarct size reduction in heat-shocked rats.
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Recent studies have shown that improved myocardial salvage after heat-shock pretreatment correlates with the amount of induced cardiac heat-shock protein (HSP)72. However, heat shock also induces myocardial catalase activity, potentially reducing free radical-mediated ischemic injury. The
The independent effects of oxygen radical scavengers on canine infarct size. Reduction by superoxide dismutase but not catalase.
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Previous studies demonstrated a significant reduction of ultimate infarct size in the canine heart by the combined administration of superoxide dismutase plus catalase. This study was performed to assess the independent effects of each enzyme on ultimate infarct size due to ischemia/reperfusion.
Changes in levels of lipid peroxides and activity of superoxide dismutase and catalase in diabetes associated with myocardial infarction.
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Studies were carried out on the metabolism of lipid peroxides and antioxidative enzymes during diabetes and diabetes superimposed with myocardial infarction. Diabetes was induced using alloxan and myocardial infarction was induced by isoproterenol. In the case of diabetic animals there was a
Low erythrocyte catalase enzyme activity is correlated with high serum total homocysteine levels in Tunisian patients with acute myocardial infarction.
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An imbalance between pro-oxidants and antioxidant systems has been suggested to be implicated in the physiopathology of acute myocardial infarction (AMI). We aimed to evaluate the antioxidant capacity in Tunisian patients and to assess the possible relationship between erythrocyte
Effect of superoxide dismutase plus catalase on myocardial infarct size in rabbits.
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A previous study by the authors showed that myocardial infarct size in the rabbit, measured after 45 mins of ischemia and 3 h of reperfusion, could be limited by administration of superoxide dismutase (SOD) plus catalase. The present study examined whether this infarct size limitation is sustained
Evidence against the "early protection-delayed death" hypothesis of superoxide dismutase therapy in experimental myocardial infarction. Polyethylene glycol-superoxide dismutase plus catalase does not limit myocardial infarct size in dogs.
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We previously found that superoxide dismutase (SOD) did not limit myocardial infarct size after 40 or 90 minutes of ischemia and 4 days of reperfusion in dogs. Because some other studies have shown limitation of infarct size after shorter periods of reperfusion, we postulated that our negative
High- and low-dose superoxide dismutase plus catalase does not reduce myocardial infarct size in a subhuman primate model.
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Oxygen free radical scavengers have been found to decrease infarct size in dogs subjected to myocardial ischemia-reperfusion injury. A baboon open-chest model was used to determine if superoxide dismutase (SOD), an oxygen free radical scavenger, together with catalase would be equally effective in
Superoxide dismutase plus catalase therapy delays neither cell death nor the loss of the TTC reaction in experimental myocardial infarction in dogs.
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Studies to test whether superoxide dismutase (SOD), with or without catalase, limits myocardial infarct size have produced conflicting results. Positive results following short periods of reperfusion vs negative results following longer periods of reperfusion could be explained if either: (1)
Failure of superoxide dismutase and catalase to alter size of infarction in conscious dogs after 3 hours of occlusion followed by reperfusion.
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Superoxide dismutase (SOD) and catalase (CAT), enzymes that degrade superoxide anion and hydrogen peroxide, respectively, reduce size of infarction in anesthetized, open-chest dogs subjected to coronary occlusion followed by reperfusion. To evaluate potential protective effects of these enzymes in
"Reperfusion injury" by oxygen-derived free radicals? Effect of superoxide dismutase plus catalase, given at the time of reperfusion, on myocardial infarct size, contractile function, coronary microvasculature, and regional myocardial blood flow.
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Do oxygen-derived free radicals, generated at the time of reperfusion, lethally injure viable, previously ischemic myocardium, damage vascular endothelium, and impair recovery of postischemic contractile function? To address these issues, 23 anesthetized open-chest dogs underwent 2 hours of left
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