Acute Effects Of Smoking Research Articles

Acute effect of smoking on gallbladder emptying and refilling in chronic smokers and nonsmokers: A sonographic study

To ultrasonographically evaluate the acute effects of smoking on gallbladder contraction and refilling in chronic smokers and nonsmokers. Fifteen chronic smokers (21-30 years old) and fifteen nonsmokers (21-35 years old) participated in this study. Chronic smokers were selected among the volunteers who had been smoking for at least 5 years and 10 cigarettes per day (mean 17.5/d). Examinations were performed in two separate days. In the first day, basal gallbladder (GB) volumes of volunteers were measured after 8-h fasting. After the examinations, participants had a meal containing at least 30-40 gram fat. Gallbladder volume was assessed at 5, 15, 30, 60, 120 and 180 min after the meal. In the second day, participants smoked 2 cigarettes after 8-h fasting. Then, they had the same meal, and gallbladder measurements were repeated at the same time points. Same procedures were applied to both groups. The mean starving GB volumes were 23.3 +/- 3.3 mL in the first day, 21.9 +/- 3.0 mL in the second day in nonsmoker group and 18.3 +/- 3.0 mL in the first day, 19.5 +/- 2.8 mL in second day in smoker group. There was no significant difference between starving GB volumes. We did not find any significant difference between the GB volumes measured at 5, 15, 30, 60, 120 and 180 min in the first and second days in nonsmoker group. In smokers, post cigarette GB volume was found significantly higher at 5, 15 and 30 min which corresponded to GB contraction phase (P < 0.05). Control GB volume measurements were not significantly different between the two groups. Post-smoking GB volumes were also not significantly different between the two groups. Smoking prolongs the maximal GB emptying time both in smokers and in nonsmokers though it is not significant. It delays GB contraction in chronic smokers and causes a significant decrease in GB emptying volume. Smoking causes no significant delay in GB refilling in both smokers and nonsmokers. These effects of smoking observed in acute phase result in bile stasis in GB. Bile stasis is the underlying cause of most GB disorders in chronic process.

Cardiovascular Effects of Secondhand Smoke Nearly as Large as Those of Smoking-and How about Renal Effects?: Cardiovascular Effects of Secondhand Smoke: Nearly as Large as Smoking. Am Heart J 111: 2684-2698, 2005.

Cardiovascular Effects of Secondhand Smoke Nearly as Large as Those of Smoking-and How about Renal Effects?: Cardiovascular Effects of Secondhand Smoke: Nearly as Large as Smoking. Am Heart J 111: 2684-2698, 2005.

Effects of Low- and High-Nicotine Cigarette Smoking on Mood States and the HPA Axis in Men

The acute effects of smoking a low- or high-nicotine cigarette on hypothalamic-pituitary-adrenal (HPA) hormones, subjective responses, and cardiovascular measures were studied in 20 healthy men who met American Psychiatric Association Diagnostic and Statistical Manual IV criteria for nicotine dependence. Within four puffs (or 2 min) after cigarette smoking began, plasma nicotine levels and heart rate increased significantly (P<0.01), and peak ratings of 'high' and 'rush' on a Visual Analogue Scale were reported. Reports of 'high', 'rush', and 'liking' and reduction of 'craving' were significantly greater after smoking a high-nicotine cigarette than a low-nicotine cigarette (P<0.05). Peak plasma nicotine levels after high-nicotine cigarette smoking (23.9+/-2.6 ng/ml) were significantly greater than after low-nicotine cigarette smoking (3.63+/-0.59 ng/ml) (P<0.001). After smoking a low-nicotine cigarette, adrenocorticotropin hormone (ACTH), cortisol, dehydroepiandrosterone (DHEA), and epinephrine did not change significantly from baseline. After high-nicotine cigarette smoking began, plasma ACTH levels increased significantly above baseline within 12 min and reached peak levels of 21.88+/-5.34 pmol/l within 20 min. ACTH increases were significantly correlated with increases in plasma nicotine (r=0.85; P<0.0001), DHEA (r=0.66; P=0.002), and epinephrine (r=0.86; P<0.0001). Cortisol and DHEA increased significantly within 20 min (P<0.05) and reached peak levels of 424+/-48 and 21.13+/-2.55 ng/ml within 60 and 30 min, respectively. Thus cigarette smoking produced nicotine dose-related effects on HPA hormones and subjective and cardiovascular measures. These data suggest that activation of the HPA axis may contribute to the abuse-related effects of cigarette smoking.

Acute effects of cigarette smoking on inflammation in healthy intermittent smokers

BackgroundChronic smoking is the main risk factor for chronic obstructive pulmonary disease. Knowledge on the response to the initial smoke exposures might enhance the understanding of changes due to chronic smoking, since repetitive acute smoke effects may cumulate and lead to irreversible lung damage.MethodsWe investigated acute effects of smoking on inflammation in 16 healthy intermittent smokers in an open randomised cross-over study. We compared effects of smoking of two cigarettes on inflammatory markers in exhaled air, induced sputum, blood and urine at 0, 1, 3, 6, 12, 24, 48, 96 and 192 hours and outcomes without smoking. All sputum and blood parameters were log transformed and analysed using a linear mixed effect model.ResultsSignificant findings were: Smoking increased exhaled carbon monoxide between 0 and 1 hour, and induced a greater decrease in blood eosinophils and sputum lymphocytes between 0 and 3 hours compared to non-smoking. Compared to non-smoking, smoking induced a greater interleukin-8 release from stimulated blood cells between 0 and 3 hours, and a greater increase in sputum lymphocytes and neutrophils between 3 and 12 hours.ConclusionWe conclude that besides an increase in inflammation, as known from chronic smoking, there is also a suppressive effect of smoking two cigarettes on particular inflammatory parameters.

Acute and Chronic Effects of Smoking on the Arterial Wall Properties and the Hemodynamics in Smokers with Hypertension

Background and Objectives：Smoking increases cardiovascular risk and it is known to acutely increase arterial stiffness in healthy smokers. We investigated the acute and chronic effects of smoking on the arterial mechanics in smokers with hypertension. Subjects and Methods：To evaluate the acute effects of smoking, the heart rate (HR), brachial blood pressure (BP), ankle systolic BP, heart-carotid pulse wave velocity (hcPWV), heartfemoral PWV (hfPWV), femoral-ankle PWV (faPWV), heart-brachial PWV (hbPWV), and the ankle-brachial index (ABI) were measured in male hypertensive smokers (n=22, 42±2 years, mean±SEM) and in normotensive smokers (n=30, 39±1 years) before and 5, 10 and 15 minutes after smoking 1 cigarette (nicotine content: 0.9 mg). To evaluate the chronic effects of smoking, we compared the HR, brachial BP, PWVs, ABI and carotid intima-media thickness (IMT) between the normotensive smokers and nonsmokers (n=32, 37±1 years), and also between the hypertensive smokers and nonsmokers (n=21, 48±2 years). Results：Smoking induced significant acute increases of the HR, brachial BP and hfPWV in the normotensive and hypertensive smokers (p 0.05). The magnitude of the increase in the HR, brachial BP and hfPWV after smoking were not different between the hypertensive and normotensive smokers. There was no significant differences (p>0.05) between the chronic normotensive smokers and the nonsmokers, and also between the hypertensive smokers and the non-smokers. Conclusion：Smoking acutely increased the HR, brachial BP and aortic stiffness in hypertensive smokers and normotensive smokers, and it had a more significant impact on the femoral arterial stiffness in the hypertensive smokers than in the normotensive smokers. However there were no significant chronic effects of smoking on the hemodynamics, arterial stiffness and carotid IMT. Our findings suggest that the acute increase in aortic and femoral arterial stiffness after smoking may contribute to the increased incidence of adverse cardiovascular events in smokers with hypertension. (Korean Circulation J 2005;35:493-499)

Effects of Erdosteine on Smoking-Induced Lipid Peroxidation in Healthy Smokers

Oxidative stress caused by smoking has been implicated in many pulmonary diseases. Smoking causes reductions in plasma nitrate plus nitrite (NOx) concentrations and increases in plasma malondialdehyde (MDA) concentrations, which indicate oxidative stress and lipid peroxidation, respectively. In this study, we investigated the acute effects of smoking a single cigarette on the plasma concentrations of NOx and thiobarbituric acid reactive substances (TBARS) including MDA, and whether administration of erdosteine, a mucolytic and antioxidant agent, affects these parameters. Thirty healthy smokers were included in the study. Subjects smoked a single cigarette in 10 minutes on the study day. For analysis of NOx, TBARS and cotinine, blood was drawn from each subject before and 5 and 30 minutes after smoking. The subjects were then randomly divided into two groups, one receiving placebo and the other erdosteine suspension 175mg/5mL twice daily for 1 month. After this treatment period, the same study protocol was carried out. Two subjects in the placebo and five subjects in the study group were excluded because of noncompliance. Twenty-three (14 female, 9 male) subjects completed the study. Their mean age was 32 +/- 8 years and their smoking history was 14 +/- 9 pack-years. Baseline NOx, TBARS and cotinine concentrations were similar between the groups. NOx concentrations decreased significantly after smoke exposure. At the end of the treatment period there were no significant differences in NOx, TBARS or cotinine concentrations between the groups. The concentration of TBARS after smoking decreased significantly in the erdosteine-treated group (at 5 minutes: 2.8 +/- 0.5 micromol/L before treatment and 2.3 +/- 0.3 micromol/L after treatment, p < 0.05; at 30 minutes: 2.8 +/- 0.5 micromol/L before treatment and 1.8 +/- 0.7 micromol/L after treatment, p < 0.05). Smoking history was significantly correlated with cotinine concentrations. Acute smoke exposure decreased plasma NOx concentrations in healthy smokers, and this was not changed with erdosteine treatment. However, significant decreases were noted in TBARS concentrations after smoke exposure in the group that received erdosteine, suggesting that short-term erdosteine administration might help prevent smoking-induced lipid peroxidation.

Smoking and caffeine have a synergistic detrimental effect on aortic stiffness and wave reflections

We investigated the acute and chronic combined effect of cigarette smoking and caffeine intake on aortic stiffness and wave reflections. We have shown that smoking and caffeine separately increase arterial stiffness. Aortic stiffness and wave reflections are important determinants of the efficient performance of the cardiovascular system and prognosticators of cardiovascular risk. The acute effects of smoking (one cigarette), caffeine (200 mg, equivalent to 2 cups of coffee), and smoking plus caffeine were studied in 24 healthy subjects according to a randomized, placebo- and sham procedure-controlled crossover design. The chronic effect of smoking and caffeine was studied in a population study that enrolled 160 healthy subjects. Acute study: there was a significant interaction between caffeine and smoking with regard to pulse-wave velocity (p < 0.01) and augmentation index (p < 0.05). When smoking followed caffeine intake, pulse-wave velocity and augmentation index increased further by 0.52 m/s and 13.4%, respectively, reaching a total of 0.85 m/s and 17.4%, 0.17 m/s and 9.2% in excess of the mere sum of caffeine effect (0.33 m/s and 4%) alone and smoking effect alone (0.35 m/s and 4.2%). Population study: there was a significant interaction of chronic coffee consumption and smoking regarding pulse-wave velocity (p < 0.05) and augmentation index (p = 0.001). The present study shows, for the first time, that when smoking and caffeine intake are combined, they interact and exert a synergistic, unfavorable effect on aortic stiffness and wave reflections on both an acute and chronic basis.

P.1.080 Assessment of cerebral regions associatedwith sexual arousal in depressive women before and after antidepressant treatment by using BOLD-fMRI

Chronic nicotine treatment has deleterious effects on vascular functioning and catecholamine modulation, which may compromise erectile functioning. Evidence that long-term cigarette smoking is an independent risk factor for introducing impotence is robust. However, limited studies have focused on the acute effects of smoking on physiological sexual response, and none have investigated the deleterious effects of isolated nicotine on human sexual arousal. Consequently, pathophysiological underpinnings of tobacco-induced—and particularly, nicotine-induced—erectile dysfunction are not well understood.To provide the first empirical examination of the acute effects of isolated nicotine on sexual arousal in nonsmoking men.Twenty-eight sexually functional heterosexual men (mean age 21 years), each with less than 100 direct exposures to nicotine, participated in a double-blind, randomized, placebo-controlled, crossover trial. Participants received either Nicorette polacrilex gum (SmithKline Beecham Consumer Healthcare, Pittsburgh, PA, USA) (6 mg; approximately equivalent to smoking one high-yield cigarette) or placebo gum, matched for appearance, taste, and consistency, approximately 40 minutes prior to viewing an erotic film.Physiological (circumferential change via penile plethysmography) and subjective (continuous self-report) sexual responses to erotic stimuli were examined, as well as changes in mood.Nicotine significantly reduced erectile responses to the erotic films (P = 0.02), corresponding to a 23% reduction in physiological sexual arousal. This occurred in 16 of 20 men with valid physiological recordings. Nicotine had no significant effect on continuous subjective ratings of sexual arousal (P = 0.70) or on mood (all Ps > 0.05).Isolated nicotine can significantly attenuate physiological sexual arousal in healthy nonsmoking men. These findings have implications for elucidating physiological mechanisms responsible for the effects of nicotine on sexual dysfunction, and for assisting public health policy in considering the deleterious effects of nicotine on sexual health. Harte CB, and Meston CM. Acute effects of nicotine on physiological and subjective sexual arousal in nonsmoking men: A randomized, double-blind, placebo-controlled trial.

Acute Cigarette Smoking-Induced Hemodynamic Alterations in the Common Carotid Artery-A Transcranial Doppler Study-

Cigarette smoking has been shown to temporarily alter cerebral flow velocity and vasomotor reactivity, so the aim of this study was to assess the acute effects of smoking a single cigarette on the common carotid artery (CCA) hemodynamics in healthy nonsmokers. Using a 7.0 MHz linear transducer of a computed sonography system, the CCA hemodynamics, including the diameter of the left and right CCA, peak systolic velocity, maximum end-diastolic velocity, time-averaged maximum velocity pulsatility index, resistivity index, flow volume, diameter and area of the CCAs, were measured in 16 healthy nonsmokers before and immediately after smoking a cigarette. Compared with the baseline, heart rate and blood pressure significantly increased, the diameter, flow volume and area of each CCA were unchanged, and the pulsatility index and resistivity index were significantly altered after smoking. In addition, the peak systolic velocity, maximum end-diastolic velocity and time-averaged maximum velocity were significantly altered after smoking. Cigarette smoking significantly altered the CCA hemodynamics in nonsmokers, probably as a consequence of enhanced adrenergic activity.

392 Echocardiographic assessment of coronary flow reserve in patients with borderline stenosis of LAD. Comparison with exercise echocardiography

Backgrounds and Objectives: The effects of smoking on coronary blood flow has not been well evaluated. Coronary blood flow velocity (CFV) can be measured directly with transthoracic Doppler echocardiography (TTDE) and conducted immediately after smoking. The purpose of this study was to evaluate the chronic and acute effects of smoking on CFV and coronary blood flow reserve (CFR). Methods: The study population consisted of 20 healthy men (11 smokers and 9 non-smokers). None of this study participants had a history of cardiovascular disease or other risk factors for coronary artery disease except smoking. Smoking was abstained at least 4 hours before study in smokers. CFV was measured at the distal left anterior descending coronary artery by TTDE at baseline and during intravenous adenosine infusion (140ug/kg/min) in all subjects. In smokers, immediately after two consecutive cigarettes smoking, CFV was measured repeatedly at baseline and during adenosine infusion. CFR after smoking was corrected with rate pressure product (RPP) because of marked alteration of heart rate and blood pressure after smoking. Results: Before smoking, CFR and coronary vascular resistance index (CVRI) did not differ between non-smokers and smokers (CFR:3.5 ± 0.8 vs 3.6 ± 0.6, p>0.05, CVRI:0.28 vs 0.28, p>0.05). The acute effect of smoking on coronary blood flow is shown below.

A study of the acute effect of smoking on cerebral blood flow using 99mTc-ECD SPET

Cigarette smoking is known to be associated with atherosclerosis, is an important risk factor for stroke and has other serious effects. The aim of this study was to evaluate the acute effect of cigarette smoking on cerebral blood flow using statistical parametric mapping (SPM). Ten healthy volunteers with a smoking habit were studied using technetium-99m-labelled ethylcysteinate dimer single-photon emission tomography (SPET). We evaluated the regional cerebral blood flow under the smoking and resting states. The regional cerebral blood flow on smoking-activated SPET was significantly decreased in the whole brain as compared with that on resting SPET. Our findings therefore suggest that one of the acute effects of cigarette smoking is to induce a diffuse decrease in cerebral blood flow.

Cigarette smoking is associated with an acute impairment of microvascular function in humans

An effect on microvascular function has been proposed as a possible mechanism explaining the association of acute smoking with increased blood pressure and decreased insulin sensitivity. However, the effects of smoking on microvascular function have not been studied. We have investigated the acute effects of smoking on microvascular function in 12 healthy smokers. Before and after smoking a cigarette, we measured heart rate, blood pressure and capillary recruitment during peak reactive hyperaemia. We also measured endothelium-dependent and endothelium-independent vasodilatation of the skin microcirculation with iontophoresis of acetylcholine and sodium nitroprusside respectively combined with laser Doppler fluxmetry. To exclude non-specific changes, a control study with sham smoking was performed. The smoking and sham smoking studies were conducted in a randomized order. Compared with sham smoking, acute smoking caused increases in heart rate (smoking, 9.3±4.1beats/min; sham, -1.3±3.0beats/min; P&lt;0.001) and systolic blood pressure (smoking, 6.3±8.8mmHg; sham, 0.8±4.4mmHg; P&lt;0.05); decreases in absolute (smoking, -4.9±6.9 per mm2; sham, 0.8±2.1 per mm2; P = 0.01) and relative (smoking, -13.8±21.4%; sham, 1.9±6.9%; P = 0.02) capillary recruitment during peak reactive hyperaemia; and decreases in absolute [smoking, -62.4±47.7 perfusion units (PU); sham, -30.8±32.6PU; P = 0.04] and relative (smoking, -147±163%; sham, 32±225%; P = 0.07) vasodilatation caused by acetylcholine. Absolute (smoking, -31.6±58.5PU; sham, -8.4±44.0PU; P = 0.3) and relative (smoking, -50.2±219.0%; sham, -17.1±139%; P = 0.7) vasodilatation caused by sodium nitroprusside were not affected. Thus acute smoking is associated with impaired capillary recruitment during peak reactive hyperaemia and impaired microvascular endothelium-dependent vasodilatation. These findings may explain the increased blood pressure and decreased insulin sensitivity that have been observed after acute smoking.

Acute effects of smoking on diastolic function in healthy participants: Studies by conventional doppler echocardiography and doppler tissue imaging

The acute effects of smoking on left ventricular (LV) function were studied in 36 healthy participants (mean age 38 ± 10 years). The studies were made before and immediately and 30 minutes after smoking a cigarette. From apical 4- and 2-chamber views, the mitral annular velocities, determined by pulsed wave Doppler tissue imaging, were measured at 4 LV sites corresponding to the septum and the anterior, lateral, and inferior walls. A mean value from the 4 sites was used to assess LV function. The peak systolic, early diastolic, late diastolic, and the ratio of early to late diastolic velocities were recorded. In addition, other conventional Doppler echocardiographic diastolic parameters were also determined. Heart rate was increased immediately after smoking (from 67 ± 8 to 74 ± 10 bpm, P < .001). There was no change in systolic mitral annular velocity. Diastolic LV function was changed significantly immediately after smoking. The transmitral A wave increased (0.55 ± 0.1 vs 0.7 ± 0.1 m/s, P < .001), the transmitral E/A ratio decreased (1.5 ± 0.6 vs 1.1 ± 0.3, P < .001), and the transmitral E-wave deceleration time increased (186 ± 42 vs 211 ± 44 ms, P < .05). The diastolic myocardial velocity at the mitral annulus also changed significantly: the early diastolic velocity decreased (16 ± 3 vs 15 ± 3 cm/s, P < .001), the late diastolic velocity increased (10.9 ± 2.2 vs 12 ± 2.4 cm/s, P < .001), and the ratio of early to late diastolic annular velocities decreased (1.5 ± 0.5 vs 1.2 ± 0.4, P < .001). The changes in the transmitral flow velocities remained unaltered even 30 minutes afterward, although the heart rate returned to normal. The results were similar in both smokers and nonsmokers. Acute smoking of a cigarette influences LV diastolic function in healthy participants. The mechanism behind this effect cannot be explained only by changes in the heart rate or loading conditions. The mechanism is probably more complex. (J Am Soc Echocardiogr 2002;15:1232-7.)

Nitric oxide but not carbon monoxide is continuously released in the human nasal airways.

Results from different laboratories indicate that nitric oxide (NO) and carbon monoxide (CO) coexist in the human airways both in health and disease. These gases are present in exhaled human breath and high concentrations of NO as well as CO have been reported in the nasal airways. In addition, exhaled CO and NO are increased in patients with airways inflammation. NO and CO were measured simultaneously in orally exhaled air and in air sampled from the nose in 18 healthy subjects using chemiluminescence (for NO) and infrared (for CO) techniques at different fixed flow rates. The acute effects of smoking on airway release of NO and CO were also studied. Nasal NO was detected in all subjects and the concentrations were highly flow-dependent (mean+/-SEM: 236+/-23 and 527+/-49 parts per billion (ppb), at 2 and 0.5 L x min(-1), respectively). In contrast, no evidence of CO release in the nasal airways regardless of sample flow rate was found. In fact, additional experiments indicated a net absorption of CO when low levels of this gas were flushed through the nasal cavity. Nasal CO also remained undetectable after smoking. Both NO (22+/-2 ppb) and CO (1.1+/-0.1 parts per million) were consistently found in orally exhaled air. CO, but not NO, levels increased acutely after smoking a cigarette. The authors conclude that the patterns of nitric oxide and carbon monoxide release in the airways seem to differ profoundly in healthy subjects. Orally exhaled air contains both nitric oxide and carbon dioxide whereas nasal air contains nitric oxide only.

Effects of cigarette smoking on psychopathology scores in patients with schizophrenia: An experimental study

Cigarette smoking and/or nicotine administration have been shown to transiently ameliorate several psychophysiological deficits in patients with schizophrenia such as indicators of deficient sensory gating and attention, but acute effects of smoking on positive and negative symptoms in schizophrenia have not been evaluated in experimental paradigms. The current study assessed whether smoking of cigarettes, after 6–12 h abstinence, transiently alters the expression of negative and/or positive symptoms in patients with schizophrenia who have a history of regular smoking. In a double‐blind, placebo controlled study patients with schizophrenia participated in two sessions in which they smoked either cigarettes moderately high in nicotine content or denicotinized cigarettes. They were interviewed pre‐and postsmoking to obtain ratings of PANSS and SANS scales, and had blood pressure and pulse serially recorded before and after smoking. Pulse rate and blood pressure were slightly higher after smoking in the high nicotine cigarette session. Negative symptom scores on both scales were significantly lower after cigarette smoking compared to same‐day predrug baseline, but there were no differences in active versus denicotinized cigarette drug effects. These results suggest that acute smoking of cigarettes reduces negative symptoms in patients with schizophrenia in this experimental paradigm. Future work needs to identify the mechanism responsible for this behavioral effect.

Effects of stress and behavioral interventions in hypertension--the effects of smoking and nicotine replacement therapy on blood pressure.

Effects of stress and behavioral interventions in hypertension--the effects of smoking and nicotine replacement therapy on blood pressure.

Acute effects of smoking on human cerebral blood flow: a transcranial Doppler ultrasonography study.

Middle cerebral artery (MCA) flow velocity was continuously monitored during smoking in an observational study (n = 14) using transcranial Doppler (TCD) ultrasonography. Cerebral autoregulatory vasodilator capacitance under inspired CO2 challenge was also measured before smoking and at peak smoking effect. Several puffs on a single lighted cigarette over a period of five minutes acutely increased MCA mean flow velocity in every subject (group mean increase: 19%, individual increases ranged 2-64%) with a response onset and offset detectable within several seconds of beginning and ending smoking. The mechanism for the increase in MCA flow velocities appeared to be independent of the CO2 autoregulatory mechanism. Gender subgroup analysis showed smoking acutely suppressed the CO2 vasodilator capacitance by 56% in men but only by 5% in women (p = 0.05). The magnitude of the acute smoking-induced increases in MCA flow velocities appeared to be independent of the estimated cigarette yields for nicotine, carbon monoxide, and "tar." Smoking in healthy subjects acutely increased MCA mean flow velocity, which may reflect a global increase in cerebral blood flow via complex influences on the cerebral autoregulation.

The acute influence of tobacco smoking on adhesion molecule expression on monocytes and neutrophils and on circulating adhesion molecule levels in vivo

Soluble adhesion molecules have been reported as risk markers of a wide range of human diseases and specific adhesion molecules may play a direct role in pathological processes. Serum soluble intercellular adhesion molecule-1 (sICAM-1) is known to be significantly elevated in smokers compared to non-smokers. We examined the acute effects of smoking a standard 2R1 research cigarette on the serum concentration of sICAM-1 and other circulating adhesion molecules (sP-selectin, sE-selectin, sL-selectin, sVCAM-1 and sPECAM-1) in heavy smokers (serum cotinine >/= 100 ng/ml), light smokers (serum cotinine </= 60 ng/ml) and non-smokers (serum cotinine </= 10 ng/ml) by ELISA. Adhesion molecule expression on the cell surface of monocytes and neutrophils in peripheral blood was examined by flow cytometry. The sICAM-1 concentration directly correlated to serum cotinine concentration (p= 0.047) and nicotine load (p= 0.033) in smokers and was significantly elevated compared to non-smokers (p= 0.037). Other than a decrease in the concentration of sP-selectin over 1 hour regardless of smoking, no significant temporal alterations of any adhesion molecule were observed following the smoking experience or in the non-smoking control group. No significant difference in surface expression of ICAM-1, CD18, PECAM-1 or L-selectin on peripheral monocytes or neutrophils was observed over a 1-hour period following smoking. These data suggest that the elevated concentration of sICAM-1 in smokers is not due to an immediate effect of smoking.

The influence of acute smoking on leucocytes, platelets and the endothelium

Cigarette smoking is a risk factor for the development of atherosclerosis. Possible mechanisms for this include leucocytes and platelet activation, and/or damage to the endothelium, any of which may contribute to changes in thrombosis and haemostasis. We examined the acute effects of smoking on these systems by obtaining blood before, immediately after, and at 10 and 30 min after the rapid smoking of two cigarettes in sequence by 20 smokers. Blood samples taken at the same time points from ten non-smokers acted as control material. In the smokers there was a transient rise in leucocyte count and neutrophil activation, but von Willebrand factor (VWF—marking endothelial damage) increased steadily at each time point ( P<0.05). There were no changes in neutrophil elastase, soluble intercellular adhesion molecule-1 (sICAM-1—normally increased in smokers), fibrinogen, platelet count or soluble P-selectin (marking platelet activation, also normally increased in smokers). We conclude that the acute smoking of two cigarettes in succession will activate leucocytes and cause endothelial cell damage, but will not immediately influence platelet activity.

Acute Effects of Cigarette Smoking on Platelet Function and Plasma Catecholamines in Hypertensive and Normotensive Men

In this randomized controlled crossover study essential hypertensive men (n = 13) and matched normotensive controls (n = 18) were examined before and during cigarette and sham smoking to assess the acute effects of smoking on platelets and plasma catecholamines. Platelet activity in vivo was determined by measurements of the released α-granule constituent β-thromboglobulin (β-TG) in plasma and in urine. Urinary high molecular weight β-TG and venous plasma epinephrine increased significantly during smoking in the hypertensive group, but not among the normotensive men. Thus, cigarette smoking induces a mild platelet release reaction and also elicits a significantly higher epinephrine response in hypertensive men compared to normotensive controls.