Time and dose effect of transdermal nicotine on endothelial function (original) (raw)
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Contribution of nicotine to acute endothelial dysfunction in long-term smokers
Journal of the American College of Cardiology, 2002
The aim of this study was to determine whether nicotine, a constituent of cigarette smoke, contributes to acute endothelial dysfunction after smoking one cigarette. BACKGROUND Animal studies suggest that nicotine might cause an impairment of endothelium-dependent vasodilation via an increase in oxidative stress.
The effect of nicotine on aortic endothelium
Atherosclerosis, 1987
This study used quantitative electron microscopy to assess ultrastructural features of endothelial injury occurring with exposure to nicotine. Fourteen mice were given nicotine in their drinking water for 5 weeks. The dose (5 mg/kg body wt/day) was equivalent to a human smoking 50-100 cigarettes/day. A control group of mice [12] was unexposed to nicotine over the same period. Stereological analysis of electron micrographs of endothelium from both groups revealed that the nicotine-exposed endothelium showed greater cytoplasmic vacuolation, mitochondrial swelling and subendothelial oedema than the control endothelium. In addition the intercellular cleft morphology was significantly (P < 0.005) less complex than in the control endothelium. This difference in cleft morphology suggests the nicotine-exposed endothelium is more permeable than the control endothelium. The ultrastructural differences noted in this study are indicative of endothelial damage, and provide structural evidence to support the hypothesis that nicotine contributes to the pathogenesis of arterial disease in smokers.
Circulation, 2001
Background-The mechanisms involved in the dysfunction of both endothelium-dependent vasodilatation (EDV) and NO biosynthesis related to smoking are unclear. In this study, EDV was assessed in healthy smokers and nonsmokers in vivo and, using serum from the same individuals, was related to the NO biosynthetic pathway in vitro. Methods and Results-Flow-mediated EDV of the brachial artery was measured in 23 male patients (8 nonsmokers and 15 smokers). Serum was collected, added to confluent (Ϸ85%) monolayers of human umbilical vein endothelial cells (HUVECs), and incubated for 12 hours. Basal and substance P-stimulated NO production was measured. The HUVECs used for measuring basal NO production were lysed, and both endothelial NO synthase (eNOS) protein expression and eNOS activity were determined. EDV was lower in smokers compared with nonsmokers (PϽ0.001). HUVECs treated with serum from smokers compared with nonsmokers showed significantly lower basal (PϽ0.0001) and stimulated (PϽ0.02) NO production, higher eNOS expression (PϽ0.0001), but lower eNOS activity (PϽ0.004). There was a significant positive correlation between in vivo EDV and in vitro substance P-stimulated NO production (rhoϭ0.57, PϽ0.01) and between basal NO production and eNOS activity (rϭ0.54, PϽ0.008) and a negative correlation between basal NO production and eNOS protein expression (rϭϪ0.60, PϽ0.003). Conclusions-This is the first study to combine an in vivo model with a near-physiological in vitro model to demonstrate an association between decreased NO production and reduced EDV. Cigarette smoking was associated with reduced EDV, NO generation, and eNOS activity in the presence of increased eNOS protein expression. (Circulation. 2001;104: 1905-1910.)
Effects of chronic oral consumption of nicotine on the rabbit aortic endothelium
The American journal of pathology, 1981
New Zealand white rabbits (10) were administered daily doses of nicotine (2.4 mg/kg/day) in their drinking water for 25 weeks. Nicotine-treated rabbits were compared with control rabbits (10) in terms of blood serum biochemistry and lipid profiles, blood cells counts, changes in aortic endothelial cell morphologic characteristic and distribution, and vessel wall permeability (Evans blue dye uptake). Fasting serum levels of glucose, triglycerides, total cholesterol, and LDL-cholesterol were elevated in nicotine-treated rabbits. No significant differences (nicotine vs control) were seen in leukocyte, erythrocyte and platelet counts, or hematocrit and hemoglobin. Control and nicotine-treated rabbit aortas showed similar focal areas of increased Evans blue dye uptake; staining was localized primarily to aortic arch areas. Endothelial cells (luminal surface) from non-Evans blue and Evans blue arch areas were examined by a combination of Häutchen preparation (silver-stained vessels) and s...
Coronary vascular responses to nicotine In anaesthetized dogs
European Journal of Pharmacology, 1990
The effect of the intra-coronary (i. c.) injection of nicotine on large coronary artery diameter and coronary blood flow was examined in anaesthetized dogs. In sixteen untreated dogs nicotine (20 gg i. c.) had a biphasic effect on arterial pressure (initial increase, 7 ___ 2 mmHg; secondary decrease, -8 + 3 mmHg) which was accompanied by small and variable effects on heart rate and an increase in LV dP/dt. Nicotine increased large coronary artery diameter by 5.8 ± 0.8% but had a biphasic effect on coronary blood flow (initial increase, 41 ± 7 ml/min; secondary decrease, -10 4-2 ml/min). Bilateral vagotomy or muscarinic receptor blockade with atropine (0.1 mg/kg i.v.) did not significantly affect the nicotine-induced changes in coronary artery diameter or coronary blood flow. The additional antagonism of fladrenoceptors with propranolol (1 mg/kg i.v.) abolished the effect of nicotine in coronary artery diameter (A CD =0.2 ± 0.2%) and the initial increase in coronary blood flow (A CBF = 1 ___ 1 ml/min) but enhanced the secondary decrease in flow (A CBF = -25 ± 3 ml/min). The nicotine-induced decrease in coronary blood flow observed after muscarinic and fl-adrenoceptor blockade was attenuated by antagonism of et-adrenoceptors with prazosin (10 gg/kg i.c., A CBF =--15 4-3 ml/min) and abolished after additional antagonism of e2-adrenoceptors with idazoxan (50 ~tg/kg i.c., A CBF = -2 ± 1 ml/ rain). These results indicate that in the anaesthetized dog intra-coronary injection of nicotine results in fl-adrenoceptor mediated dilatation of both large and small coronary arteries. In the coronary resistance vessels, but not in the large coronary artery, the dilatation is opposed by etand e2-adrenoceptor mediated vasoconstriction.
Endothelial Dysfunction in Healthy Passive Smoker
Indonesian Journal of Cardiology, 2013
Introduction. Passive smoking may have a deleterious effect to cardiovascular system and subsequent enormous public health implication. The sidestream cigarette smoke suggest impaired endothelial production of nitrit oxide. Since endothelial dysfunction is an early feature of atherogenesis, early detection on this become important and hopefully can prevents the subsequent atherosclerlotic events. There were only few studies have assessed the effects of passive smoking to human arterial wall. The objective of this study was to detect endothelial dysfunction in healthy passive smokers young adults. Methods. We studied 80 healthy subjects 20 to 35 years old,which were divided into two groups, consist of 32 passive smokers and 48 subjects as controls. Passive smokers were defined as non-smokers who had been exposed to environmental tobacco smoke for at least one hour daily for three or more years. Endothelial function was measured by response of flow-mediated vasodilatation in brachial...