ArticleBMC cardiovascular disorders2006
Lipid-soluble smoke particles damage endothelial cells and reduce endothelium-dependent dilatation in rat and man.
Article in BMC cardiovascular disorders, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Tobacco smoking and vascular biology and function: evidence from human studies.Pflugers Archiv : European journal of physiology · 2023Article
- The effect of subchronic cigarette smoke exposure on oxidative stress parameters and endothelial nitric oxide synthase in a rat aorta.ARYA atherosclerosis · 2021Article
- Preventive effect ofF1000Research · 2021Article
- Can enhanced external counter pulsation as a non-invasive modality be useful in patients with ischemic cardiomyopathy after coronary artery bypass grafting?The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2018Article
- Omega-3 Polyunsaturated Fatty Acids Protect Against Cigarette Smoke-Induced Oxidative Stress and Vascular Dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Smoking Behaviors and Arterial Stiffness Measured by Pulse Wave Velocity in Older Adults: The Atherosclerosis Risk in Communities (ARIC) Study.American journal of hypertension · 2016Article
- Chronic nicotine treatment enhances vascular smooth muscle relaxation in rats.Acta pharmacologica Sinica · 2015Article
- The effects of Secondhand Smoke (SHS) exposure on microvascular endothelial function among healthy women.Tobacco induced diseases · 2015Article
- Cigarette smoke and inflammation: role in cerebral aneurysm formation and rupture.Mediators of inflammation · 2012Review
- Protecting against vascular disease in brain.American journal of physiology. Heart and circulatory physiology · 2011Review
- Cigarette exposure induces changes in maternal vascular function in a pregnant mouse model.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries.Vascular health and risk management · 2009Article
- Enhanced external counter pulsation in treatment of refractory angina pectoris: two year outcome and baseline factors associated with treatment failure.BMC cardiovascular disorders · 2008Article
- Cigarette smoking leads to reduced relaxant responses of the cutaneous microcirculation.Vascular health and risk management · 2008Article
- Smoking particles enhance endothelin A and endothelin B receptor-mediated contractions by enhancing translation in rat bronchi.BMC pulmonary medicine · 2006Article
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4 authors.
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Abstract
backgroundCigarette smoking is a strong risk factor for vascular disease and known to cause dysfunction of the endothelium. However, the molecular mechanisms involved are still not fully understood.
methodsIn order to reveal the direct effects of lipid-soluble smoke particles on the endothelium, ring segments isolated from rat mesenteric arteries and human middle cerebral arteries (MCA) obtained at autopsy were incubated for 6 to 48 hrs in the presence of dimethylsulphoxide (DMSO)-soluble particles from cigarette smoke (DSP), i.e. lipid-soluble smoke particles. The endothelial microstructure was examined by transmission electron microscopy. The endothelial function was evaluated by acetylcholine (ACh)-induced endothelium-dependent vasodilatation, using a sensitive myograph.
resultsAfter DSP treatment, the arterial endothelium was swollen and loosing its attachment. In functional tests, the total ACh-induced dilatation, the nitric oxide (NO)-mediated and the endothelium-derived hyperpolarization factor (EDHF)-mediated dilatations were significantly decreased by DSP in a time- and concentration-dependent manner (p < 0.05). Nicotine, an important compound in cigarette smoke had, in an equivalent concentration as in DSP, no such effects (p > 0.05). Similar results were obtained in the human MCA.
conclusionThus, we demonstrate that the lipid-soluble smoke particles, but not nicotine, caused damage to arterial endothelium and reduced the endothelium-dependent dilatation in man and rat.
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