The effect of cigarette smoke, nicotine, and carbon monoxide on the permeability of the arterial wall

Allen, David R.; Browse, N L; Rutt, D L; Butler, L.; Fletcher, C.

doi:10.1067/mva.1988.avs0070139

Cited by 18 publications

(13 citation statements)

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“…Similar doses in chronic exposure (> 7 but ≤ 21 days) did not alter extravasation of macromolecules in human pulmonary epithelium (Minty et al . 1984), canine femoral endothelium (Allen et al . 1988), hamster cheek pouch microvessels (Myers et al .…”

Section: Discussionmentioning

confidence: 99%

Chronic nicotine exposure alters blood–brain barrier permeability and diminishes brain uptake of methyllycaconitine

Lockman

Schyf

Abbruscato

et al. 2005

Journal of Neurochemistry

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Methyllycaconitine (MLA) is reported to be a selective antagonist for the nicotinic acetylcholine receptor a7 subtype and has been found in animal behavioral studies to reduce nicotine self-administration and attenuate nicotine withdrawal symptoms. While MLA crosses the blood-brain barrier (BBB), no studies have assessed brain uptake in animals subjected to chronic nicotine exposure. Given that chronic nicotine administration has been reported to alter BBB parameters that may affect the kinetic BBB passage of MLA, we evaluated MLA brain uptake in naive and S-(-)nicotine-exposed rats (4.5 mg/kg/day for 28 days; osmotic minipumps) using in situ rat brain perfusions. Our results demonstrate that in situ 3 H-MLA brain uptake rates in naive animals approximate to intravenous kinetic data (K in , 3.24 ± 0.71 · 10 )4 mL/s/g).However, 28-day nicotine exposure diminished 3 H-MLA brain uptake by $60% (K in , 1.29 ± 0.4 · 10 )4 mL/s/g). This reduction was not related to nicotine-induced 3 H-MLA brain efflux or BBB transport alterations. Similar experiments also demonstrated that the passive permeation of 14 C-thiourea was diminished $24% after chronic nicotine exposure. Therefore, it appears that chronic nicotine exposure diminishes the blood-brain passive diffusion of compounds with very low extraction rates (i.e. permeability-limited compounds). These findings imply that the pharmacokinetics of neuropharmaceutical agents that are permeability limited may need to be re-evaluated in individuals exposed to nicotine.

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Section: Discussionmentioning

confidence: 99%

Chronic nicotine exposure alters blood–brain barrier permeability and diminishes brain uptake of methyllycaconitine

Lockman

Schyf

Abbruscato

et al. 2005

Journal of Neurochemistry

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“…Nearly all smokers exhibit raised fibrinogen levels that increase with age [32, 33] and correlations between fibrinogen level and smoking status have previously been described [15, 31, 34, 35]. The plasma fibrinogen level is a significant factor in the genesis of atherosclerotic changes [36–38], and in animal experiments a significant increase in the permeability coefficients, allowing increased permeation of fibrinogen into the vascular endothelium, occurred during administration of tobacco smoke and CO, but not during nicotine infusions [39]. Similarly, one study in humans reported a significant drop in the carboxyhaemoglobin (COHb) level after smoking was discontinued for 3 days (1.70 vs. 5.65%), and the COHb levels did not increase when nicotine was administered via transdermal patches [40].…”

Section: Discussionmentioning

confidence: 99%

Effects of cigarette smoking or nicotine replacement on cardiovascular risk factors and parameters of haemorheology

Haustein¹,

Krause²,

Haustein³

et al. 2002

Journal of Internal Medicine

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Objectives. Cigarette smoking causes cardiovascular (CV) disease, but the relative roles of nicotine and other components of tobacco smoke remain unclear. We investigated the effect of stopping smoking, by using nicotine replacement therapy (NRT), on haemorheology parameters. Design. Open, parallel-group trial (intervention group and control smokers). Setting. Clinic within university department of pharmacology. Subjects. One hundred and ninety-seven males, aged 25-45 years, smoking >20 cigarettes per day. Interventions. One hundred and sixty-four subjects were instructed to stop smoking and received NRT for 12 weeks and 33 acted as controls. After 12 weeks, NRT was discontinued, and all subjects were followed-up at 26 weeks. At the end of the study, the NRT group was divided into abstainers (self-reported, verified by exhaled carbon monoxide <10 ppm) and relapsers, who were unable to remain abstinent. Main outcome measures. Plasma viscosity, fibrinogen, erythrocyte deformability, reactive capillary blood flow, transcutaneous partial oxygen tension (tcpO 2 ) and haematocrit, assessed at 4, 8, 12, and 26 weeks. Results. After 6 months, plasma fibrinogen (9.95 vs. 8.24 lmol L -1 at baseline; P < 0.003), reactive capillary flow (t-p max : 9.3 vs. 11.2 s at baseline; P < 0.005), and tcpO 2 (50.4 vs. 34.9 mmHg at baseline; P < 0.0001) were significantly improved in abstainers, but changes in plasma viscosity and erythrocyte deformability were inconclusive. Other CV risk factors, such as haematocrit and white blood cell count, decreased to a greater extent in abstainers than in relapsers. Expired carbon monoxide concentrations reflected the changes in smoking and decreased in abstainers from 30.4 ppm at baseline to 4.2 ppm; P < 0.0001). Conclusions. Smoking cessation improved CV parameters, and use of nicotine medications did not negate these improvements.

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“…Tobacco inhalation results in vascular endothelial damage leading to inflammation and increased secretion of cell adhesion molecules with subsequent increased platelet and monocyte adhesion to the vessel wall. The result is to promote atherosclerosis [35–37]. With respect to lipoproteins, smoking disturbs lipoprotein metabolism by increasing insulin resistance and lipid intolerance and is implicated in the production of small‐dense LDL, which is more readily oxidized.…”

Section: Cigarette Smokingmentioning

confidence: 99%

The molecular genetics of cardiovascular disease: clinical implications

Stephens

Humphries

2003

Journal of Internal Medicine

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The effect of cigarette smoke, nicotine, and carbon monoxide on the permeability of the arterial wall

Cited by 18 publications

References 0 publications

Chronic nicotine exposure alters blood–brain barrier permeability and diminishes brain uptake of methyllycaconitine

Chronic nicotine exposure alters blood–brain barrier permeability and diminishes brain uptake of methyllycaconitine

Effects of cigarette smoking or nicotine replacement on cardiovascular risk factors and parameters of haemorheology

The molecular genetics of cardiovascular disease: clinical implications

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