Platelet Sensitivity to Prostacyclin in Smokers and Non-smokers

Burghuber, Otto Chris; Punzengruber, Christian; Sinzinger, H.; Haber, Paul; Silberbauer, K

doi:10.1378/chest.90.1.34

Cited by 94 publications

(48 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…25 Notably, many of the above effects are caused by passive smoking. [3][4][5]8 Definitive evidence about the atherogenic nature of CSmodified LDL is its interaction with cultured human macrophages, which store cholesterol and develop to foam cells. The cholesteryl esterification reaction reflects the amount of cholesterol stored in these cells.…”

Section: Discussionmentioning

confidence: 99%

“…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%

See 1 more Smart Citation

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

1998

View full text Add to dashboard Cite

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.)

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

1998

View full text Add to dashboard Cite

show abstract

“…4,5,19,31,32,32a Platelet activation in response to SHS was first evaluated in an experiment that exposed smokers and nonsmokers to 20 minutes of SHS (Table 2). 31 At baseline, platelet activation among smokers was higher than activation in nonsmokers. After the experiment, activation remained the same in smokers but was significantly increased in nonsmokers, to the point that their platelet activation was not discernibly different from that of the smokers.…”

Section: Platelet Functionmentioning

confidence: 95%

Cardiovascular Effects of Secondhand Smoke

2005

View full text Add to dashboard Cite

Background-Secondhand smoke increases the risk of coronary heart disease by Ϸ30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers. Methods and Results-We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system-platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size-is exquisitely sensitive to the toxins in secondhand smoke.

show abstract

“…For example, Kritz and Sinzinger (30) observed an increase in markers of platelet activation and a decrease in platelet sensitivity to PGI2 among 12 nonsmokers exposed for 20-min in an 18 m3 room in which 30 Gitanes had recently been smoked. The hypercoagulable state demonstrated among nonsmokers acutely exposed to ETS (30)(31)(32)(33)(34) resembles the acute changes in smokers who consume one or two cigarettes after a period of abstinence (35)(36)(37)(38)(39)(40)(41)(42)(43). Schmid et al (31) found that, prior to ETS exposure, the platelets of nonsmokers were significantly less activated than those of smokers, whereas after 20 min exposure to ETS, platelet activation increased among the nonsmokers exposed to ETS (p < 0.01) but remained constant among the active smokers (p > 0.05).…”

Section: Experimental Studies Ofets Exposurementioning

confidence: 99%

Why Is Environmental Tobacco Smoke More Strongly Associated with Coronary Heart Disease Than Expected? A Review of Potential Biases and Experimental Data

Howard¹,

Thun²

1999

Environmental Health Perspectives

View full text Add to dashboard Cite

Despite exposure levels estimated to be equivalent to smoking only 0.1-1.0 cigarettes per day, exposure to environmental tobacco smoke (ETS) is estimated to increase the risk of death from coronary heart disease (CHD) between 25 and 35% above the risk of nonexposed persons. This surprisingly large risk associated with a seemingly small exposure has raised doubts about the validity of attributing the increased CHD risk to ETS exposure. This paper reviews various biases that have been hypothesized to account for the increased CHD risk associated with ETS in the epidemiologic studies and characterizes the adverse effects of ETS on thrombosis, vascular endothelium, and exercise tolerance observed in experimental studies of humans and laboratory animals. None of the identified factors that has been proposed to introduce a spurious association between ETS and heart disease seem to invalidate the epidemiologic findings, either separately or in combination. In addition, experimental studies of ETS and heart disease demonstrate that acute exposure of humans and other species to ETS affects platelet function, vascular endothelium, and myocardial exercise tolerance at exposure concentrations widely prevalent in the workplace. Because exposure to ETS affects multiple physiologic pathways, it appears biologically plausible that ETS could cause the substantial increase in CHD risk that has been observed in epidemiologic studies. Key words: atherosclerosis, cardiovascular disease, risk factor, smoking. -Environ Health Perspect 1 07(suppl 6): 853-858 (1999). http.//ehpnet 1. niehs. nih.gov/docs/1999/suppl-6/853-858howard/abstract. html

show abstract

Platelet Sensitivity to Prostacyclin in Smokers and Non-smokers

Cited by 94 publications

References 24 publications

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

Cardiovascular Effects of Secondhand Smoke

Why Is Environmental Tobacco Smoke More Strongly Associated with Coronary Heart Disease Than Expected? A Review of Potential Biases and Experimental Data

Contact Info

Product

Resources

About