Effects of monoamine oxidase inhibitors on isoproterenol-induced cardiomegaly in rats

Stanton, H.C.; Bowman, Zelia; Cooper, C

doi:10.1016/0041-008x(70)90182-1

Cited by 8 publications

(8 citation statements)

References 9 publications

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“…Pretreatment with monoamine oxidase inhibitors significantly ameliorates the severity of myocardial injury produced by ISO treatment. This action was reflected by improved biochemical events [Stanton et al 1970;Singh et al 1980]. Aspirin treatment decreases the biochemical lesions which occur due to the activation of lipid peroxidation and also normalizes the antioxidant defence enzymes such as α-glycerophosphate dehydrogenase (GDP), glutathione S-transferase, SOD, and catalase (Table 1) [Manjula et al 1994].…”

Section: Antioxidative Agentsmentioning

confidence: 99%

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Garg

Kumari

2014

Therapeutic Advances in Cardiovascular Disease

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High incidences of myocardial infarction associated with high morbidity and mortality, are a major concern and economic burden on industrialized nations. Persistent β-adrenergic receptor stimulation with isoproterenol leads to the development of oxidative stress, myocardial inflammation, thrombosis, platelet aggregation and calcium overload, which ultimately cause myocardial infarction. Therapeutic agents that are presently employed for the prevention and management of myocardial infarction are beta-blockers, antithrombotics, thrombolytics, statins, angiotensin converting enzyme inhibitors, angiotensin II type 1 receptor blockers, calcium channel blockers and nitrovasodilators. In spite of effective available interventions, the mortality rate of myocardial infarction is progressively increasing. Thus, there has been a regular need to develop effective therapies for the prevention and management of this insidious disease. In this review, the authors give an overview of the consequences of isoproterenol in the pathogenesis of cardiac disorders and various therapeutic possibilities to prevent these disorders.

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Section: Antioxidative Agentsmentioning

confidence: 99%

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Garg

Kumari

2014

Therapeutic Advances in Cardiovascular Disease

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“…Microscopic methods (17,20,19,8) are tedious and their utilization in experiments with a large number of animals is limited. Macroscopic evaluation (17, 9) of heart lesions is affected by subjective error and is applicable to lesions of higher degree.…”

Section: Discussionmentioning

confidence: 99%

Studies on isoprenaline-induced myocardial lesions 1. Quantitative evaluation by Mercurascan uptake

Mráz

Kronrád

et al. 1977

Basic Res Cardiol

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For the quantitative evaluation of myocardial damage induced by isoprenaline (ISO) a method based on the uptake of 203Hg-labelled Mercurascan (MSC) in the heart was used. The increase of myocardial uptake of MSC in ISO-treated rats over control values was very rapid and might be directly proportional to the number of damaged myocardial cells actually present in the heart. MSC-uptake method of myocardial damage evaluation was more sensitive and precise than other methods tested (macroscopic evaluation according to Rona, increase of heart weight). Different modifications of MSC-uptake test may be selected in relation to experimental conditions. MSC test is especially useful for evaluation of early myocardial lesions induced by small doses of ISO (0.01 mg/kg).

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“…Accordingly, in an experimental model in rats, it has been demonstrated that myocardial oxidative stress could be partially prevented by MAO inhibitors [100]. …”

Section: Mitochondria and Cocaine-induced Cardiovascular Toxicitymentioning

confidence: 99%

Cardiovascular Mitochondrial Dysfunction Induced by Cocaine: Biomarkers and Possible Beneficial Effects of Modulators of Oxidative Stress

Graziani

Sarti

Arese

et al. 2017

Oxidative Medicine and Cellular Longevity

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Cocaine abuse has long been known to cause morbidity and mortality due to its cardiovascular toxic effects. The pathogenesis of the cardiovascular toxicity of cocaine use has been largely reviewed, and the most recent data indicate a fundamental role of oxidative stress in cocaine-induced cardiovascular toxicity, indicating that mitochondrial dysfunction is involved in the mechanisms of oxidative stress. The comprehension of the mechanisms involving mitochondrial dysfunction could help in selecting the most appropriate mitochondria injury biological marker, such as superoxide dismutase-2 activity and glutathionylated hemoglobin. The potential use of modulators of oxidative stress (mitoubiquinone, the short-chain quinone idebenone, and allopurinol) in the treatment of cocaine cardiotoxic effects is also suggested to promote further investigations on these potential mitochondria-targeted antioxidant strategies.

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Effects of monoamine oxidase inhibitors on isoproterenol-induced cardiomegaly in rats

Cited by 8 publications

References 9 publications

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Studies on isoprenaline-induced myocardial lesions 1. Quantitative evaluation by Mercurascan uptake

Cardiovascular Mitochondrial Dysfunction Induced by Cocaine: Biomarkers and Possible Beneficial Effects of Modulators of Oxidative Stress

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