Effect of Propranolol on Oxidative Processes of Heart Muscle

Gvozdják, J; Gvozdjáková, A; Bada, V

doi:10.1159/000169346

Cited by 11 publications

(11 citation statements)

References 3 publications

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“…1 It has been suggested that acute exposure to passive smoking deteriorates oxygen delivery and use in the myocardium, 2 causes mild coronary vasoconstriction, 3 increases platelet activity in nonsmokers, 4 and damages the endothelium, indicated by the appearance of anuclear endothelial cell carcasses in the blood. 5 Long-term exposure to passive smoking reduces the serum level of ascorbic acid, 6 impairs the arterial endothelial function probably through impaired endothelial nitric oxide activity, 7 and increases the thickness of the carotid wall.…”

mentioning

confidence: 99%

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

1998

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Background-According to the American Heart Association, passive smoking is an important risk factor for coronary heart disease (CHD), but the mechanisms underlying this association are not fully understood. We studied the acute effect of passive smoking on the factors that influence the development of CHD: the antioxidant defense of human serum, the extent of lipid peroxidation, and the accumulation of LDL cholesterol in cultured human macrophages, the precursors of foam cells in atherosclerotic lesions. Methods and Results-Blood samples were collected during 2 ordinary working days from healthy, nonsmoking subjects (nϭ10) before and after (up to 5.5 hours) spending half an hour in a smoke-free area (day 1) or in a room for smokers (day 2). Passive smoking caused an acute decrease (1.5 hours after exposure) in serum ascorbic acid (PϽ.001) and in serum antioxidant defense (PϽ.001), a decreased capacity of LDL to resist oxidation (PϽ.01), and the appearance of increased amounts of lipid peroxidation end products in serum (PϽ.01). Finally, LDL isolated from subjects after passive smoking was taken up by cultured macrophages at an increased rate (PϽ.05). Conclusions-Exposure of nonsmoking subjects to secondhand smoke breaks down the serum antioxidant defense, leading to accelerated lipid peroxidation, LDL modification, and accumulation of LDL cholesterol in human macrophages. These data provide the pathophysiological background for the recent epidemiological evidence about the increased CHD risk among passive smokers. (Circulation. 1998;97:2012-2016.)

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confidence: 99%

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

1998

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“…Also NIC. interrupted the mitochondrial respiratory chain causing enhanced production of superoxide anions and hydrogen peroxide [5]. All these factors play an important part in the progression of lipid peroxidation and elevated levels of MDA (lipid peroxidation end products).…”

Section: Discussionmentioning

confidence: 99%

“…Smoking induces an inflammatory response in the lung and shows a role in progression of obstructive pulmonary diseases (COPD) with a main influence on the health care sources, in the developed and developing countries [3,4]. NIC interrupts the mitochondrial respiratory chain causing an elevated liberation of hydrogen peroxide and superoxide anions [5]. NIC can enhance lipid peroxidation and cause depletion of antioxidants during induction of experimental vascular endothelial dysfunction [6].…”

Section: Introductionmentioning

confidence: 99%

Agmatine Ameliorates Nicotine Induced Lung Injury in Rats through Decrease TGF-ß1 and Bax Immunoexpression and by Anti-oxidative Sress Pathway: Histological, Immunohistochemical and Biochemical Study

Attia¹,

Nader²,

Elmansy³

et al. 2017

J Cytol Histol

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“…All together these pathological alterations characterize the pattern of the experimental cardiomyopathy [26][27][28][29] . There is a clear evidence that myocardial necrosis and vascular changes are the anatomical substrate of chronic damage from smoking.…”

Section: H R O N I C E X P O S U R E a N D T Y P E O F Damagementioning

confidence: 99%

Current and Controversial Features of Cardiovascular Damage from Cigarette Smoking

Leone

2016

Journal of Cardiology and Therapy

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A great number of studies have undoubtedly demonstrated that cardiovascular damage from cigarette smoking cannot be denied, although some controversies on the topic still exist. The damage to the heart and blood vessels is initially characterized by transient functional alterations consisting of endothelial dysfunction, reduced exercise tolerance, increased systolic blood pressure and heart rate following acute exposure. On the contrary, chronic exposure to smoking develops, at the time, firstly reversible and, then, irreversible lesions mainly involving myocardium with an ischemic damage and smoke cardiomyopathy as well as coronary, carotid and cerebral arteries, which display atherosclerotic pathology. The analysis of the epidemiological studies on cardiovascular damage support the controversies on the effects of smoking, because not the same alterations are sometimes observed in different studies on the topic. However, when standardized experimental procedures are followed, the same alterations are clearly reproduced showing that cardiovascular damage from cigarette smoking cannot be denied.

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Effect of Propranolol on Oxidative Processes of Heart Muscle

Cited by 11 publications

References 3 publications

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

Agmatine Ameliorates Nicotine Induced Lung Injury in Rats through Decrease TGF-ß1 and Bax Immunoexpression and by Anti-oxidative Sress Pathway: Histological, Immunohistochemical and Biochemical Study

Current and Controversial Features of Cardiovascular Damage from Cigarette Smoking

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