Acute Effect Of Smoking Research Articles

Thrombopoietin contributes to enhanced platelet activation in cigarette smokers

Objectives: Thrombopoietin (TPO) is a humoral growth factor that primes platelet activation in response to several agonists. We recently showed that TPO enhances platelet activation in unstable angina and sepsis. Aim of this study was to investigate the role of TPO in platelet function abnormalities described in cigarette smokers. Methods: In a case–control study we enrolled 20 healthy cigarette smokers and 20 nonsmokers, and measured TPO and C-reactive protein (CRP), as well as platelet–leukocyte binding and P-selectin expression. In vitro we evaluated the priming activity of smoker or control plasma on platelet activation, and the role of TPO in this effect. We then studied the effects of acute smoking and smoking cessation on TPO levels and platelet activation indices. Results: Chronic cigarette smokers had higher circulating TPO levels than nonsmoking controls, as well as increased platelet–leukocyte binding, P-selectin expression, and CRP levels. Serum cotinine concentrations correlated with TPO concentrations, platelet–monocyte aggregates and P-selectin expression. In addition, TPO levels significantly correlated with ex vivo platelet–monocyte aggregation and P-selectin expression. In vitro, the plasma from cigarette smokers, but not from nonsmoking controls, primed platelet–monocyte binding, which was reduced when an inhibitor of TPO was used. We also found that acute smoking slightly increased TPO levels, but did not affect platelet–leukocyte binding, whereas smoking cessation induced a significant decrease in both circulating TPO and platelet–leukocyte aggregation. Conclusion: Elevated TPO contributes to enhance platelet activation and platelet–monocyte cross-talk in cigarette smokers.

Effect of Smoking Cessation on Visually Evoked Cerebral Blood Flow Response in Healthy Volunteers

Background/Aims: In our previous study, impaired visually evoked flow velocity response was demonstrated in young chronic smokers. Our aim was to study whether impaired cerebrovascular reactivity is reversible 6–18 months after smoking cessation. Methods: Flow velocity changes, evoked by visual stimulus, were recorded in the posterior cerebral arteries in 15 smokers, 15 former smokers and 15 nonsmokers. The stimulation protocol consisted of 10 cycles with a resting phase of 20 s (baseline) and a stimulating phase of 40 s for each cycle. Relative changes of flow velocity were expressed in relation to baseline. Breath holding index, visual evoked potential and intima-media thickness were also examined. Results: Repeated measures ANOVA revealed marked difference in the flow velocity time courses between the 3 groups (p < 0.01). The flow response was significantly worse in former smokers than in nonsmokers (p < 0.002), however, no significant difference was found between former and current smokers (p = 0.0556). Conclusion: This is the first transcranial Doppler study demonstrating long-term impairment of visually evoked cerebrovascular response after smoking cessation. These findings indicate that the impairment of neurovascular coupling caused by smoking is due to structural changes of the vessels, rather than acute effect of smoking.

Acute Maximal Exercise and the Vasodilatory Capacity of Young Cigarette Smokers

PURPOSE: The primary purpose of this study was to compare the vasodilatory response to reactive hyperemia (RH) at rest and following maximal exercise in otherwise healthy cigarette smokers and healthy non-smokers. In addition we examined the vasodilatory response to RH of cigarette smokers following acute exposure to cigarette smoke both at rest and following maximal exercise. METHODS: The vasodilatory capacity of 19 cigarette smokers (CS) (23 ± 2 years) and 19 non-smokers (NS) (23 ± 3 years) was assessed using strain-gauge plethysmography on the forearm following RH before and after a maximal treadmill test. Peak forearm blood flow (FBF) and area under the curve (AUC) of the FBF response at rest and following exercise were compared between CS and NS using repeated measures ANOVA. On a separate visit, cigarette smokers were asked to smoke one cigarette twenty minutes prior to testing in order to examine the effects of acute smoking (AS) compared to non-acute smoking (NAS). RESULTS: At rest, the CS group demonstrated a 23% reduction in peak FBF response to RH compared to the NS group (15.8 ± 2.9 CS vs. 20.6 ± 5.5 NS mL/min/100mL, p < 0.05) and a 22% reduction in AUC of the FBF response to RH (607 ± 225 CS vs. 775 ± 233 NS mL/min/100mL x min, p = 0.058). The CS group also had a 26% reduction in AUC of the FBF response to RH on the AS visit compared to the NAS visit (449 ± 147 AS vs. 607 ± 225 NAS mL/min/100mL x min, p < 0.05). However, following maximal exercise, no significant differences in peak or AUC of the FBF response were found between the CS and NS groups. Also, no differences were observed following maximal exercise between visits (AS vs. NAS) in the CS group. CONCLUSION: These findings support the beneficial effect of exercise on the vasodilatory response of young healthy cigarette smokers, as acute maximal exercise resulted in a similar FBF response to RH in the CS and NS groups, despite the fact that the CS group exhibited an impaired FBF response to RH prior to exercise.

Acute Effects of Cigarette Smoking on Arterial Stiffness and Blood Pressure in Male Smokers With Hypertension

Although the acute increase of arterial stiffness and blood pressure (BP) after cigarette smoking in healthy smokers is considered a possible mechanism of increased cardiovascular risk, the acute effect of smoking on arterial stiffness in hypertensive smokers is unknown. We investigated the acute effects of cigarette smoking on arterial stiffness and BP in hypertensive male smokers. Heart rate (HR), brachial and ankle BP, and pulse-wave velocity (PWV) were measured in 22 hypertensive male smokers (HTs) and in 30 normotensive male smokers (NTs) before and 5, 10, and 15 min after smoking one cigarette (nicotine content, 0.9 mg). Smoking induced acute increases of HR, brachial BP, and heart-femoral PWV (hfPWV) in NTs and HTs (P < .05). Ankle systolic BP and femoral-ankle PWV were acutely increased in HTs (P < .05), but not in NTs. In HTs, brachial systolic BP and hfPWV at 15 min were higher than at baseline (P < .05). An acute increase of hfPWV in the HTs was significant (P = .025) after adjustment for total cholesterol, time-dependent HR, and brachial mean arterial pressure, but acute changes of other PWVs lost statistical significance. Cigarette smoking acutely increases aortic stiffness and BP in male smokers with hypertension, and the effects persist longer than in male smokers without hypertension.

Effects of acute smoking on brain activity vary with abstinence in smokers performing the N-Back Task: A preliminary study

We previously reported that compared with a non-deprivation state, overnight abstinence from cigarette smoking was associated with higher brain activity in the left dorsolateral prefrontal cortex (L-DLPFC) during a low demanding working memory challenge, and little increase beyond this activity level during more taxing working memory conditions. In the present study, we aimed to assess how recent smoking (overnight abstinence vs. smoking ad libitum) influenced the effect of smoking a cigarette on brain activity related to a working memory challenge. Six smokers performed the N-Back working memory task during functional magnetic resonance imaging (fMRI) both before and after smoking a cigarette in each of two test sessions: one following overnight abstinence from smoking (∼ 13 h) and the other following ad libitum smoking. Task-related activity in L-DLPFC showed a significant interaction between the effects of acute smoking, test session, and task load. After overnight abstinence, post-smoking brain activity in L-DLPFC was lower than before smoking at low task load and higher at high task load; corresponding activity on a day of ad libitum smoking was higher at low load and lower at high task load after smoking during the session. These data suggest that the effect of acute smoking on working memory processing depends on recent prior smoking and task load. In particular, they provide preliminary evidence that functional efficiency of working memory is improved by smoking a cigarette during abstinence, while the effect of a cigarette in a non-deprived state varies with the nature and difficulty of the working memory challenge. This interaction merits further examination in larger studies specifically designed to consider this issue.

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.

The effect of tobacco smoke ingredients on immunity with special reference to chronic obstructive pulmonary disease

Tobacco smoke consists of several thousand toxic and carcinogenic substances . Ingredients of tobacco smoke have numerous extremely harmful effects on human health and are related to the occurrence of various diseases such as respiratory infections, chronic obstructive pulmonary disease (COPD) and lung cancer . The insreased incidence of these diseases in smokers is possibly caused by the effects of tobacco on the function disorder of the immune system. Whereas the acute effect of smoking on the function of the immune system is less known, chronic exposure to tobacco ingredients causes a decreased function of T-lymphocytes . Nowadays it is considered by the World Health Organization (WHO) that smoking cessation is the single most effective and cost effective way to reduce exposure to COPD risk factors . Tobacco smoke might affect the function of the immune system . Numerous studies in vitro and in vivo have demonstrated so far that there is an immunosuppresive effect of tobacco smoke on T and B-lymphocytes 6, . During smoking, a smoker inhales both the smoke and the particles. Among the particles inhaled, a thousand of ingredients are taken in the most important of which are nicotine, various carcinogenes, metals and others. Nicotine is the main immunosuppressive ingredient of tobacco smoke . Numerous investigations have demonstrated that tar and nicotine have an extremely toxic effect on the immune system . The effect of tobacco smoke ingredients on immunity depends on the doses of substances, as well as on the duration of exposure. Investigations of effects of tobacco smoke on the function of the immune system

The Effect of Acute Smoking on Spinal Fusion: An Experimental Study Among Rabbits

The establishment of an environment to force animals to inspire cigarette smoke is mandatory to study the true effects of smoking. This model has been used to study long-bone healing but has not yet been used to study spinal fusion. Forty male rabbits were divided into four equal groups. All the animals underwent bilateral intertransverse-process fusion at L5-L6 using the 1995 fusion model of Boden et al. The first (C8-week) group did not undergo cigarette smoke inhalation and individual rabbits were killed at 8 weeks; the second (S8-week) group underwent intermittent cigarette smoke inhalation and individual rabbits were killed at 8 weeks; the third (C6-week) group did not undergo cigarette smoke inhalation, and animals were killed at 6 weeks; and the fourth (S6-week) group underwent intermittent smoke inhalation and group-included rabbits were killed at 6 weeks. Subsequent to the animals having been killed, the fusion masses were harvested for a series of studies including manual palpation, biomechanical testing, radiographic examination, and histologic analysis. Six rabbits died shortly after the operation. Of the remaining 34 rabbits, the lumbar spine specimen was harvested for study. Manual palpation, radiographic examination, and histologic analysis of the fusion masses revealed no statistically significant difference in fusion results between the control and the corresponding smoking group killed at either 8 weeks or 6 weeks. Biomechanical testing of the fusion masses also revealed no statistically significant difference in fusion results between the control and the smoking group killed at 8 weeks, although it did indicate that smoking resulted in a 44% decrease in mean flexion stiffness and a 32% decrease in mean extension stiffness among the animals killed at 6 weeks. The former (decrease in flexion stiffness) was statistically significant (p < 0.05). The results of the biomechanical testing conducted as a part of the current study demonstrate that acute cigarette smoke inhalation delays but does not prevent the spinal fusion process for rabbits.

Association of Hypoadiponectinemia With Smoking Habit in Men

Adiponectin is emerging as an important molecule in obesity, the metabolic syndrome, and cardiovascular disease. On the other hand, smoking habit is well known to be related to cardiovascular disease and hypertension. To examine the association between adiponectin concentration and smoking habit, we performed an epidemiological survey and an acute exposure test in humans and an experiment in adipocytes to elucidate the mechanism underlying the association between adiponectin and smoking. In the epidemiological study, we enrolled a total of 331 male subjects to examine chronic smoking exposure. Plasma adiponectin was significantly lower (P=0.01) in current smokers (5.3+/-0.3 microg/mL) than in never-smokers (6.5+/-0.4 microg/mL). A significant association between smoking and low adiponectin level was also confirmed in multiple regression analysis including age, body mass index, hypertension, diabetes, hyperlipidemia, and creatinine clearance (never-smokers 6.5+/-0.4 microg/mL; past smokers 5.6+/-0.3 microg/mL; current smokers 5.2+/-0.4 microg/mL; F=4.52; P=0.01). To examine the acute effect of smoking on adiponectin concentration for 12 hours, we measured plasma adiponectin level in 5 male never-smokers before smoking and 3, 6, and 12 hours after smoking, with the result that adiponectin showed a significant decrease after smoking (12 hours; -14.5+/-0.6%; P<0.01). In cultured mouse 3T3-L1 adipocytes, H2O2 and nicotine reduced the mRNA expression and secretion of adiponectin in a dose-dependent manner. Smoking habit is associated with adiponectin concentration in men, and its suppressive effect is mediated in part through direct inhibition of smoking on adiponectin expression in adipocytes.

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.

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.

The influence of cigarette smoking on circulating concentrations of antioxidant micronutrients

Cigarette smoke is a significant source of oxidative stress, one potential mechanism for its untoward health effects. The antioxidant defense system is partly comprised of antioxidant micronutrients, making it important to understand the relationship between cigarette smoking and circulating concentrations of antioxidant micronutrients. A synthesis of the literature shows that compared with nonsmokers, on average, active smokers have greater than 25% lower circulating concentrations of ascorbic acid, α-carotene, β-carotene, and cryptoxanthin. The differences in blood concentrations of these micronutrients in former smokers is intermediate between never and current smokers, but average circulating concentrations of α-carotene, β-carotene, and cryptoxanthin were 16–22% lower in former smokers compared with never smokers. Differences in dietary habits between smokers and nonsmokers could potentially account for these associations. Dietary micronutrient intake is associated with blood micronutrient concentrations. Furthermore, patterns of micronutrient consumption by smoking status mimic the pattern of associations observed for blood concentrations. For example, when pooled across studies intake of vitamin C was 16% lower in current smokers and 2% lower in former smokers than in never smokers; the corresponding figures for β-carotene were 17 and 4%, respectively. Despite the strong potential for confounding, the differences observed between current smokers and nonsmokers seem to be due to an acute effect of smoking based on results of studies of smoking and antioxidant micronutrient concentrations that have either adjusted for dietary antioxidant micronutrient intake and other potential confounding factors or documented short term changes in circulating antioxidant micronutrient concentrations in smokers before and after smoking cigarettes. The associations observed with active smoking also appear to hold true for passive smoking, implying that even low-dose exposures to tobacco smoke can result in lowered circulating antioxidant micronutrient concentrations. Smoking was more weakly associated with circulating concentrations of vitamin E and the nonprovitamin A carotenoids lutein/zeaxanthin and lycopene. The combined evidence supports the conclusion that cigarette smoking is independently associated with lowered circulating concentrations of ascorbic acid and provitamin A carotenoids. These associations have implications for the design and interpretation of epidemiologic studies of antioxidant micronutrients in relation to health and disease. To the extent that these micronutrients are associated with health and longevity, this evidence documents yet another deleterious consequence of cigarette smoking on human health.

Effects of Cigarette Smoking and Nicotine Nasal Spray on Psychiatric Symptoms and Cognition In Schizophrenia

Schizophrenic patients have among the highest rates of smoking of any group of patients. Previous studies have identified psychophysiological and potential nicotinic receptor abnormalities which may be associated with this phenomenon. The effects of acute smoking or acute administration of nicotine nasal spray, after smoking abstinence, on negative symptoms and neurocognitive function have been less extensively studied in experimental designs. This study investigated the effects of smoking of high nicotine or denicotinized cigarettes, and receiving active or placebo nicotine nasal sprays, on positive and negative symptoms and cognitive functions in schizophrenic patients. The study utilized a placebo controlled crossover experimental design with pre- and post-drug evaluations on each experimental day. Smoking high nicotine cigarettes decreased negative symptoms more than denicotinized cigarettes, but smoking neither cigarette changed scores of positive symptoms, anxiety, or depression. Active nicotine nasal spray did not differentially decrease negative symptoms compared with placebo, but did improve performance on a spatial organization task, and tended to improve some measures of verbal memory and two-choice reaction time in schizophrenic patients. Both high and denicotinized cigarettes improved performance on the spatial processing task, but there was no statistically significant differential drug (Cigarette type) effect. These results suggest that acute smoking of cigarettes may transiently decrease negative symptoms in patients with schizophrenia, but it is unclear whether this effect is attributable to nicotine, other components of cigarettes, or the act of smoking. Nicotine nasal spray may modestly improve some selected aspects of cognitive function in schizophrenia.

Do we undertreat hypertensive smokers? A comparison between smoking and non-smoking hypertensives

The acute effect of smoking is a rise in blood pressure and heart rate. Nevertheless, in several epidemiologic studies, smokers tend to have a slightly lower office blood pressure than non-smokers. We studied the 24 h ambulatory blood pressure consecutively in hypertensive smokers (> or = 10 cigarettes per day, n = 26) and hypertensive non-smokers (n = 26) to test the hypothesis that smoking is associated with a rise in ambulatory blood pressure. There was no difference between smokers and non-smokers in office blood pressure (153.8 +/- 22.2/98.5 +/- 10.6 vs 149.0 +/- 16.1/96.9 +/- 11.6 mmHg). However, we found a statistically significant higher daytime systolic and diastolic blood pressure in smokers (153.7 +/- 16.2/96.1 +/- 9.5 vs 145.0 +/- 12.1/90.1 +/- 10.0 mmHg) than in non-smokers. Differences were also found for office-daytime differences and when studying patients on pharmacological antihypertensive treatment separately. Daytime heart rate was also significantly higher in smokers (86.6 +/- 9.4 vs 76.0 +/- 10.9). We conclude that smokers tend to be undertreated in that they have a higher daytime blood pressure than do non-smokers, a difference that is not recognized by measuring office blood pressure alone. We therefore recommend 24h ambulatory blood pressure measurement in smokers with essential hypertension.

Exhaled 8-isoprostane as an in vivo biomarker of lung oxidative stress in patients with COPD and healthy smokers.

Most of the studies linking chronic obstructive pulmonary disease (COPD) with oxidative stress are in vitro, using invasive techniques, or measuring systemic oxidative stress. The aim of this study was to quantify oxidative stress in the lungs in patients with COPD and in healthy smokers, as reflected by 8-isoprostane concentrations in breath condensate. This is a noninvasive method to collect airway secretions. 8-Isoprostane is a prostaglandin-F(2alpha) isomer that is formed in vivo by free radical-catalyzed peroxidation of arachidonic acid. We also studied the acute effect of smoking on exhaled 8-isoprostane in healthy smokers. Exhaled 8-isoprostane was measured by a specific enzyme immunoassay in 10 healthy nonsmokers and 12 smokers, 25 COPD ex-smokers, and 15 COPD current smokers. 8-Isoprostane concentrations were similar in COPD ex-smokers (40 +/- 3.1 pg/ml) and current smokers (45 +/- 3.6 pg/ ml) and were increased about 1.8-fold compared with healthy smokers (24 +/- 2.6 pg/ml, p < 0.001), who had 2.2-fold higher 8-isoprostane than healthy nonsmokers (10.8 +/- 0.8 pg/ml, p < 0.05). Smoking caused an acute increase in exhaled 8-isoprostane by about 50%. Our study shows that free radical production is increased in patients with COPD and that smoking causes an acute increase in oxidative stress.

O13 The effect of acute smoking on platelet aggregometry and alpha granule degranulation

O13 The effect of acute smoking on platelet aggregometry and alpha granule degranulation

The acute effect of smoking on complexity of cardiac autonomic control after mild exercise

The acute effect of smoking on complexity of cardiac autonomic control after mild exercise

Oral contraceptive use and hemodynamic, lipid, and fibrinogen responses to smoking and stress in women.

The effects of acute smoking and oral contraceptive (OC) use on cardiovascular, lipid, and fibrinogen stress responses were examined in 52 female smokers and nonsmokers, half of whom were using OCs. Women smoked or sham-smoked a cigarette and then performed 2 stressful tasks. Stress elicited increases in total and low-density lipoprotein cholesterol, and in triglycerides among women who smoked, and in fibrinogen among all women. Smokers who used OCs had greater blood pressure increases to smoking and to stress than did smokers who did not use OCs. OC use was also associated with enhanced total peripheral resistance stress responses among women who smoked and cardiac output stress responses among women who sham-smoked. Results suggest that OC use moderates cardiovascular reactivity in smokers but not nonsmokers, enhancing vascular responsivity to smoking combined with stress and myocardial responsivity to stress alone.

Mechanisms underlying cerebrovascular effects of cigarette smoking in rats in vivo.

The effects of acute smoking on cerebral circulation are controversial. This study was designed (1) to clarify any differences between the effects of cigarette smoking and nicotine infusion and between the effects of single- and multiple-cigarette smoking on cerebral vessels and (2) to probe the mechanism(s) underlying the vascular responses. In pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats, pial vessel diameters were measured with the use of a cranial window preparation. We studied the effects of (1) 60 puffs per minute of mainstream cigarette smoke from cigarettes having 2 nicotine levels (0.1 and 1 mg per cigarette), (2) administration of nicotine (0.05 mg per body IV), and (3) repeated smoking (four 1 mg nicotine-containing cigarettes at 30-minute intervals) (n=6 each). Inhalation of smoke from a 0.1 or 1 mg nicotine-containing cigarette for 1 minute caused pial arterioles to constrict at 30 seconds (7.2% and 7.3%, respectively) and then to dilate (peak at 5 to 10 minutes; 4.6% and 17.9%, respectively). Nicotine infusion caused pial vasodilation (35.7%) without an initial vasoconstriction. Repeated smoking suppressed the pial vasodilation but not the initial vasoconstriction. The vasodilation induced by a single cigarette was greatly inhibited by pretreatment with mecamylamine or glibenclamide and attenuated by propranolol or Nomega-nitro-L-arginine methyl ester; the initial vasoconstriction was inhibited by seratrodast, a thromboxane A2 receptor antagonist (n=6 in each case). Single-cigarette smoking had a significant biphasic effect on cerebral arteriolar tone. The vasodilation was attenuated by repeated smoking. The vasodilation is most likely an effect of nicotine, at least in part mediated via sympathetic activation, NO production, and K+ channel activation. The vasoconstriction is partially due to thromboxane A2 induced by cigarette smoke.