Acute Effects Of Cigarette Smoking Research Articles

Acute effects of cigarette smoking on global cerebral blood flow (GCBF) in overnight abstinent tobacco smokers

Background/Aims The acute effects of tobacco smoking on gCBF were studied. Methods Positron emission tomography (PET) with H215O was used to measure quantitatively CBF in 10 right handed male volunteer tobacco smokers. After 12 hr abstinence, gCBF measurements (baseline, 5% CO2/95% O2, and cigarette smoking) were made. gCBF was adjusted based on the vascular reactivity to CO2 and PaCO2 during smoking. Results Mean gCBF during smoking compared with baseline did not change. However, an increase in nicotine arterial plasma correlated inversely with gCBF; gCBF increased in seven, decreased in seven, and was unchanged in five sessions. gCBF increased during smoking when baseline gCBF was low, whereas gCBF decreased when baseline gCBF was high. Conclusions Individual differences suggest important bimodal effects of smoking on the brains of different tobacco smokers. Clinical Pharmacology & Therapeutics (2005) 77, P67–P67; doi: 10.1016/j.clpt.2004.12.147

The Acute Effects of Cigarette Smoking on the Heterogeneity of Ventricular Repolarization in Healthy Subjects: The Relationship between QT Dispersion and Coronary Flow Reserve

Background and Objectives：Although cigarette smoking is a known risk factor for sudden cardiac death, little is known about the effects of smoking on the heart. The QT interval and QT dispersion prolongation have been associated with a lower ventricular fibrillation threshold and the occurrence of sudden cardiac death. Smoking has an unfavorable influence on the autonomic balance and myocardial blood flow. The objective of the current study was to evaluate the relationship between the QT dispersion and coronary flow reserve (CFR) in healthy young male subjects. Subjects and Methods：The study included a sample of 30 healthy young male cigarette smokers. The catecholamines level, QTc dispersion, heart rate variability and myocardial blood flow were measured, immediately before and 5 minutes after and during the smoking of 3 cigarettes. Results：Short-term smoking caused significant increases in the serum cortisol (10.9±4.9 vs. 15.0±7.0 μg/dL, p<0.01), serum epinephrine (0.038±0.026 vs. 0.046±0.026 ng/mL, p=0.044), heart rate (78±9 vs. 85±8 beats/min, p< 0.01), maximal QTc interval (412±22 vs. 435±20 ms, p<0.01), QTc dispersion (43±14 vs. 62±17 ms, p<0.01), LFnu (68±9 vs. 78±6%, p<0.01), LF/HF (3.25±2.15 vs. 5.22±1.89, p<0.01) and peak diastolic velocity (21.7±3.9 vs. 23.9±5.5 cm/sec, p=0.005), and a decrease in the CFR (3.71±0.56 vs. 3.42±0.76, p=0.024). The change in the QTc dispersion was closely related to the change in the CFR (r=-0.357, p=0.043). Conclusion：The present study is the first to demonstrate that the impaired coronary flow reserve after smoking may contribute to the increased inhomogeneity of ventricular repolarization in healthy young male smokers. (Korean Circulation J 2005;35:448-453)

Exhaled Nitric Oxide and Hydrogen Peroxide Concentrations in Asthmatic Smokers

Background: Cigarette smoking is associated with decreased nitric oxide (NO) production and increased oxidative stress in the airways. Exhaled NO levels are not higher in asthmatic smokers than in healthy non-smokers, and the value of exhaled NO for diagnosing asthma in smokers has been questioned. Objectives: To compare exhaled NO concentrations between healthy and steroid-naive and steroid-treated asthmatic smokers and non-smokers. To also assess the acute effect of cigarette smoking on exhaled NO and hydrogen peroxide (H₂O₂) levels in asthmatic smokers. Methods: Exhaled NO was measured by chemiluminescence and exhaled H₂O₂spectrophotometrically. In 7 steroid-naive asthmatic smokers exhaled NO and H₂O₂was measured both before and 15 min after smoking one cigarette. Data are given as median (range). Results: Exhaled NO level was significantly higher in steroid-naive asthmatic smokers than in healthy smokers [7.7 (3.4–32.5) ppb vs. 3.2 (2.0–7.2) ppb, p < 0.001]. Exhaled NO values were lower in smokers than in non-smokers both in healthy subjects and in steroid-naive asthmatic patients. Steroid-treated asthmatic smokers had a tendency for lower exhaled NO values [5.4 (1.7–12.0) ppb] compared to steroid-naive asthmatic smokers. Cigarette smoking caused an acute increase in exhaled H₂O₂concentrations together with a decrease in exhaled NO concentration. Conclusions: Our data suggest that an elevation in exhaled NO concentration is associated with asthma in smokers. This difference may be useful for diagnosing the disease in smokers, but its clinical value needs further evaluation. Acute increase in exhaled H₂O₂concentrations suggests that smoking increases the oxidative stress in the asthmatic airways.

Acute effects of maternal smoking on fetal hemodynamics

Objective: To investigate acute effects of cigarette smoking on fetal hemodynamics. Method: Sixty seven women between 32nd to 40th weeks of gestation were evaluated. Maternal blood pressure and heart rate, fetal heart rate (FHR) tracing, umbilical and fetal middle cerebral arterial (MCA) color Doppler measurements were evaluated. Pre- and postsmoking results were compared with paired t-test. Results: Maternal heart rate significantly increased after smoking. Baseline FHR and FHR variability remained unchanged. The number of participants who had a reactive NST was 60 in 67 before smoking (89.5%) and decreased to 47 after smoking (70.1%) ( p=0.009). There were no significant changes between maximum and minimum flow velocities, pulsatility index (PI), resistance index (RI) and systolic/diastolic flow ratio (S/D) of umbilical and middle cerebral arteries. Conclusion: The nicotine load of a single cigarette may be inadequate to cause a detectable decrease in utero-placental blood flow; however, smoking prior to the FHR recording may alter the FHR reactivity.

The Acute Effects of Cigarette Smoking on Vascular Reactivity and Vascular Tone

The Acute Effects of Cigarette Smoking on Vascular Reactivity and Vascular Tone

The Acute Effects of Cigarette Smoking on Vascular Reactivity and Vascular Tone

The Acute Effects of Cigarette Smoking on Vascular Reactivity and Vascular Tone

Reversible inhibition of mitochondrial complex IV activity in PBMC following acute smoking.

Smoking causes a decrease of mitochondrial complex IV activity in chronic smokers. However, it is not known if this toxic effect is due to the acute effect of cigarette smoke itself or is a secondary phenomenon related to other smoking factors. The study assessed mitochondrial respiratory chain function in peripheral blood mononuclear cells of 15 healthy nonsmoker individuals before smoking (t0), immediately after smoking five cigarettes in 45 min (t1) and 24 h later (t2). Blood carboxyhaemoglobin (COHb) and carbon monoxide concentrations in exhaled air (COEA) were determined to ascertain smoke inhalation status. After acute smoking, COHb increased from 0.5 +/- 0.3% to 3.3 +/- 1.5%, and COEA from 2.9 +/- 2.5 to 26.1 +/- 9.9 ppm. Complex II and III enzyme activities did not change along the study. Complex IV activity showed a 23% inhibition at t1 but returned to initial (to) levels at t2. A decay in oxygen consumption was observed after the correction for mitochondrial content. Lipid peroxidation of cell membranes remained unchanged. Short-time smoking causes an acute and reversible mitochondrial complex IV inhibition in human mononuclear cells. These results suggest that smoke itself is one of the causes for the decrease of complex IV activity observed in chronic smokers.

Acute effects of cigarette smoking on the QT interval in healthy smokers

This study assesses the effect of a first cigarette smoked in the morning on the QT interval duration in healthy habitual smokers after not smoking overnight. This study demonstrates that although after cigarette smoking the QT Bc values increase, the QT Fc and QT Lc values remained unchanged, and an increased sympathetic response was evident. The discrepancies between the results seen by different QT correction formulas emphasize the importance of selecting an accurate method for heart rate correction when evaluating and interpreting alterations in QT values.

A TEN MINUTES RESTING INTERVAL AFTER SMOKING SHOULD BE TAKEN FOR SAFTY EXERCISE PRESCRIPTION

We aimed to investigate the acute effects of cigarette smoking on cardiovascular systems during exhaustive exercise, comparing different time conditions of smoking exposure. Study subjects consisted of 3 male and 2 female habitual smokers (S; 25.0±3.4 yrs), and 2 male and 3 female non-smokers (NS; 22.7±1.8 yrs). All the participants performed symptom-limited maximal graded exercise on a cycle ergometer under three various conditions; non-smoking(control),5 min. after(S5) and 10 min.after(S10) smoking a cigarette. Heart rate(HR) and blood pressure(BP) were recorded every one-minute before, through, and after exercise. Rate pressure product(RPP), which is often used a parameter of myocardial oxygen uptake, was also calculated using obtained HR and systolic blood pressure(SBP). As to acute responses of HR or BP, both S and NS did not show significant differences among control, S5 and S10 with each other. In NS, however. ANOVA demonstrated significant differences in RPP after 8min.pedaling, the RPP of S5(27,900±4,174bpm.mmHg) was higher than those of control(24,028±3,952bpm. mmHg, p < 0.05) and of S10(24,532±2,627bpm. mmHg, p < 0.05) respectively. This intensity of emiently increased RPP appearance was equaled to 10.7±1.7METs, that is, also just above the anaerobic threshold(AT) levels in all the subjects. It is accepted that the cardiovascular risks derived from exercise stress tends to be higher over the AT point, where sympathetic tone just begin to be alerted. This finding observed in NS is thought to be due to combined effects of not only exercise but smoking only one cigarette. It also suggests that even in habitual smokers who are accustomed to the exposure of nicotine and carbon monoxide, higher demanded exercise immediately after smoking lager amount of cigarettes would be considered strenuous to cardiovascular systems. From the viewpoint of preventive cardiology, we insist on being keen to RPP response above the AT level intensity. In conclusion, at least 10 minutes resting interval after smoking should be taken for the safety exercise prescription.

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 Acute Effects of Cigarette Smoking on the Heterogeneity of Ventricular Repolarization in Healthy Subjects

Background and Objectives:Although cigarette smoking is a known risk factor of sudden cardiac death, little is known about the effects of smoking on the heart. QT interval and QT dispersion prolongation have been associated with a lowered ventricular fibrillation threshold and the occurrence of sudden cardiac death. The aim of this study was to clarify the acute effects of cigarette smoking on the QT interval and dispersion. Subjects and Methods:The study population consist of 30 young male cigarette smokers, (with a mean age, and body mass index of 26±2 years;and 22.3±2.1 kg/m) respectively. Standard 12-lead surface electrocardiograms were recorded, at immediately before, during, and 5 minutes after, smoking 3 cigarettes. The RR interval, maximum and minimum QT intervals, QT dispersion (QT maximum-QT minimum), and the ratecorrected QT dispersion were all evaluated. Results:The RR interval was significantly reduced after 1 cigarette smoking (885±200 vs. 730±110 ms, p<0.01). The maximal QTBc interval was significantly longer after smoking 1 cigarette (415±21 vs. 442±21 ms, p<0.01), but the minimum QTBc interval showed no significant changes (369±23 vs. 376±22 ms, p=0.11). The QTBc dispersion (40±14 vs. 52±12 ms, p<0.01) and QTFc dispersion (42±14 vs. 58±14 ms, p<0.01) were significantly increased after smoking. Conclusion:In young males, smoking acutely increases the maximum QT interval and QT dispersion. These changes may explain the higher risk of sudden cardiac death. (Korean Circulation J 2003;33(1):58-62)

Effect of acute cigarette smoking, alone or with alcohol, on gastric barrier function in healthy volunteers

Background. Smoking is a risk factor for gastroduodenal ulcer and gastric adenocarcinoma. However, the pathophysiological mechanisms induced by acute cigarette smoking in the human gastric mucosa are poorly understood. Aim. To evaluate the effect of acute cigarette smoking, alone or with alcohol, on the gastric permeability to sucrose, a specific marker of mucosal damage in the stomach. Subjects and Methods. Twenty healthy volunteers (B smokers/12 non-smokers) were studied. Each fasted subject ingested 500 ml of a 20% sucrose solution and the amount of sucrose excreted in a 5-hour urine collection was measured by gas chromatography. Four sucrose permeability tests were carried out: 1. basal, 2. while smoking 5 cigarettes, 3. after drinking 50 ml of a 40° alcoholic beverage, 4. a combination of 2+3. Results. Sucrose excretion increased after alcohol ingestion (40.5±6.0 mg vs 143.1±28.9 mg, p=0.002), but was not modified by acute cigarette smoking (34.4±5.9 mg). When alcohol and cigarettes were simultaneously consumed, the increase in alcohol-induced sucrose excretion was significantly reduced (73.1:± 16.6 mg, p=0.03). Basal sucrose excretion was similar in smokers and non-smokers. However, in acute cigarette smoking, a decrease in sucrose excretion was observed in smokers (p=0.02) but not in non-smokers. Conclusions. These results indicate that acute cigarette smoking may tighten the gastric mucosa in habitual smokers and this is associated with a smaller increase of gastric permeability induced by alcohol.

Acute effects of cigarette smoking on cerebral oxygenation and hemodynamics: A combined study with near-infrared spectroscopy and transcranial Doppler sonography

Cigarette smoking has been shown to increase cerebral blood flow velocity (CBFV) and reduce vasomotor reactivity temporarily. The aim of our study was to clarify whether this results from dilation of resistance vessels alone with subsequent increase in regional cerebral blood flow (rCBF), or an additional constriction of basal cerebral arteries. In 24 healthy smokers (mean age±S.D., 32.7±10.5 years), cerebral oxygenation and hemodynamics were monitored by transcranial Doppler sonography and near-infrared spectroscopy before, during, and after smoking a cigarette (nicotine 0.9 mg). We simultaneously recorded CBFV of both middle cerebral arteries, mean arterial blood pressure, skin blood flow, end-tidal CO 2, changes in concentration of cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin (μmol/l), and a cerebral tissue oxygenation index. Smoking increased CBFV ( p<0.01), oxyhemoglobin ( p<0.01), and total hemoglobin ( p<0.01). After smoking, the increase in CBFV and total hemoglobin persisted ( p<0.01), while oxyhemoglobin returned to baseline. Deoxyhemoglobin and cerebral tissue oxygenation index did not change during the whole procedure. During, but not after smoking, CBFV increase was correlated to ipsilateral changes in oxyhemoglobin and total hemoglobin ( p<0.05). The increase in oxyhemoglobin only during smoking and the lack of changes in deoxyhemoglobin and cerebral tissue oxygenation index indicate that smoking did not substantially increase rCBF. The smoking-induced elevation in CBFV might therefore be due to an additional constriction of the middle cerebral artery. The combined effects of smoking on basal cerebral arteries and arterioles might contribute to the increased stroke risk in smokers.

Smoking causes a dose-dependent increase in granulocyte-bound L-selectin

The mechanism by which cigarette smoking promotes atherosclerosis remains unclear but may involve the endothelium and leukocytes. We postulated a direct acute effect of cigarette smoking on the endothelium and granulocytes by measuring granulocyte expression of L-selectin (flow cytometry) and serum L- and E-selectin (ELISA) before and after smoking in 12 smokers with peripheral vascular disease (claudicants) and 12 otherwise healthy controls. Mean (S.D.) granulocyte L-selectin, expressed as mean fluorescence intensity (MFI), increased in a dose-dependent fashion from 3.58±0.67 and 3.27±0.67 in controls and claudicants, respectively, to 3.77±0.75 and 3.49±0.79 10 min after smoking two cigarettes ( p<0.002), and to 4.11±0.95 and 3.67±0.88 30 min after four cigarettes ( p<0.001). Serum L-selectin was lower in claudicants at all time points throughout the study period compared with controls ( p<0.005) but neither serum E- nor L-selectin levels changed following smoking. Smoking led to an increase in granulocyte expression of L-selectin, which may be important in granulocyte/endothelial adhesion and thus related to atherosclerosis. The lower serum L-selectin levels in claudicants, and the absence of a rise in serum adhesion molecules on smoking, suggests consumption by activated endothelial receptors that may be part of a negative feedback mechanism.

Acute cigarette smoking reduces vasodilative effect induced by sympathetic block in dogs

Background and Objectives: The aim of this study is to clarify the influence of acute cigarette smoking on vasodilation induced by sympathetic block. Methods: We measured mean arterial pressure, heart rate, left brachial artery blood flow (BABF), right femoral artery blood flow (FABF), and plasma catecholamines in dogs to examine the effect of acute cigarette smoking after stellate ganglion block (SGB). The experimental protocol was: (1) Left SGB using 1.0 mL 0.5% mepivacaine without smoking (sham smoking); and (2) left SGB using 1.0 mL 0.5% mepivacaine followed by a single cigarette smoking (nicotine 1 mg) 15 minutes after the block. Results: SGB induced a significant increase of BABF during the study (baseline, 100%; peak at 10 minutes after SGB, 176% ± 9%; P < .05) in sham smoking and a significant decrease of FABF from 10 minutes after the block to 20 minutes after sham smoking (baseline, 100%; bottom at 5 minutes after sham smoking, 82% ± 8%; P < .05). Smoking after SGB induced a significant decrease of BABF 60 minutes after smoking (baseline, 100%; 69% ± 11%; P < .05) and a significant decrease of FABF during the study (baseline, 100%; bottom at 20 minutes after smoking, 74% ± 20%; P < .05). Smoking significantly increased plasma norepinephrine and epinephrine through the study. Conclusions: Sympathetic block induces a significant increase of peripheral blood flow, but smoking produces a significant decrease in the blood flow in the SGB-induced dilated vessels. Reg Anesth Pain Med 2001;26:41-45.

The acute effects of cigarette smoking on human optic nerve head and posterior fundus circulation in light smokers.

To study the acute effects of cigarette smoking on tissue circulation in the optic nerve head (ONH) and posterior fundus in smokers with a short smoking history. Ten healthy smokers whose length of smoking history was within 2 years (age 25 +/- 1 years; smoking index (number of cigarettes smoked per day x length of smoking history in years) 16 +/- 4, mean +/- SE) were included in the study. Using the laser speckle method, normalised blur (NB) value, a quantitative index of tissue blood velocity, was measured every 0.125 s and averaged over three pulses across an area located in the temporal site of the ONH free of visible surface vessels (NBONH) and across an area located halfway between the macula and the ONH with no discrete vessels visible (NBch-ret). NBONH, NBch-ret and intraocular pressure (IOP) in one randomly chosen eye, and blood pressure (BP) and pulse rate (PR) were measured before, and 1, 5, 10, 15, 20, 25, 30, 45, 60 and 90 min after sham smoking. One week later, NBONH, NBch-ret and IOP in the same eye, and BP and PR were measured after cigarette smoking according to the same time schedule as in the control experiment. After sham smoking, no parameter showed a significant change during the experiment. Differences in NBONH from the baseline were not significant between the smoking experiment and sham smoking experiment, while NBch-ret showed a significant difference at 30 min. Inter-group difference in the time course of the difference from baseline was significant (ANOVA, p = 0.0246, 0.0021). BP and PR were significantly increased between 1 and 20 min after smoking while IOP showed no significant change at any time of measurement. In light smokers, cigarette smoking showed little effect on tissue blood velocity in the ONH and slightly decreased that in the posterior fundus, suggesting a significant increase in vascular resistance in these tissues.

Acute effects of cigarette smoking on renal hemodynamics.

Acute effects of cigarette smoking on renal hemodynamics.

Cigarette smoke and hypoxia induce acute changes in testicular and celebral microcirculation

The acute effects of cigarette smoking and hypoxia on the cerebral and testicular microcirculation were studied in anestethised adult rats. Smoking for 2 min did not influence arterial pO2, pCO2 or pH but it induced an increase in cerebral blood flow by 34% and inhibited vasomotion in the testis for about 1 h. One hour after smoke exposure apnea induced a slight increase in arterial pCO2, a significant decrease in pO2, and an increase in cerebral blood flow (CBF) by 54%. In animals not previously exposed to cigarette smoke apnea increased CBF by 121%, demonstrating that a short-term exposure to tobacco smoke influences the cerebrovascular reactivity for more than one hour. In the testis, apnea resulted in a decreased blood flow by 39% and a complete depression of vasomotion. Breathing 10% O2/90% N2 resulted in moderate hypoxia, a total disappearance of the vasomotion in the testis, a 24% decrease in testicular blood flow, but a 23% increase in CBF.Our results indicate that short- term exposure to tobacco smoke induces marked acute vascular effects in both the brain and the testis. Apnea and moderate hypoxia elicted totally differnt effect in the brain and testis, indicating different vascular control mechanisms.

Acute Reduction in Ankle/Brachial Index Following Smoking in Chronic Smokers with Peripheral Arterial Occlusive Disease

The ankle-brachial systolic pressure index (ABI), a noninvasive measure of peripheral arterial occlusive disease (PAOD) severity, is considered a marker of atherosclerosis and an independent predictor of mortality. However, it is not known whether factors other than PAOD severity, such as cigarette smoking, have an effect on ABI measurement. Therefore, the authors examined the acute effects of cigarette smoking on ABI and the peripheral circulation in 10 older (63 +/- 10 years) chronic smokers (39 +/- 37 pack-years) with PAOD (ABI=0.64 +/- 0.14). The patients were instructed to refrain from smoking and from consuming caffeine-containing beverages for at least 12 hours before the tests. The patients were randomly assigned to 2 days of testing consisting of a nonsmoking and a smoking day. Resting heart rate, blood pressure, ABI, and calf blood flow by plethysmography were obtained on both testing days. The smoking day consisted of smoking two filter cigarettes over a period of 10 minutes before the measurement of ABI and calf blood flow. The ABI on the smoking day (0.55 +/- 0.11) was lower (p=0.008) than on the nonsmoking day (0.64 +/- 0.14) owing to a lower (p=0.020) ankle systolic blood pressure (81 +/- 28 vs 93 +/- 28 mmHg). Brachial systolic blood pressures, heart rate, and calf blood flow were not altered by smoking (p>0.05). These results demonstrate that the acute effect of cigarette smoking lowers the ABI in chronic smokers with intermittent claudication, thereby yielding evidence of a transient deleterious effect of cigarette smoking on the peripheral circulation in chronic smokers.

Acute effects of cigarette smoking on tissue circulation in human optic nerve head and choroid-retina

ObjectiveTo study the acute effects of cigarette smoking on tissue circulation in the human optic nerve head (ONH) and choroid-retina. DesignNonrandomized, comparative trial (sequential self-controlled). ParticipantsNine healthy habitual smokers (age, 28 ± 4 years; number of cigarettes smoked per day, 27 ± 10; length of smoking history, 10 ± 4 years; mean ± standard deviation). InterventionUsing the laser speckle method, normalized blur (NB) value, a quantitative index of tissue blood velocity, was measured every 0.125 second and averaged over three pulses across an area located in the temporal site of the ONH free of visible surface vessels (NBONH) and across an area located halfway between the macula and the ONH with no discrete vessels visible (NBch-ret). NBONH, NBch-ret, and intraocular pressure (IOP) in one randomly chosen eye, and blood pressure (BP) and pulse rate (PR) were measured before and 1, 5, 10, 15, 20, 25, 30, 45, 60, and 90 minutes after sham smoking using a short drinking straw as a cigarette substitute (control). One week later, NBONH, NBch-ret, and IOP in the same eye, and BP and PR were measured after cigarette smoking according to the same time schedule as in the control experiment. Main outcome measuresNBONH and NBch-ret. ResultsIn the control experiment, all parameters examined showed no significant change during the experimental period. Differences in NBONH and NBch-ret before and after actual smoking were significantly greater than those in the control experiment (analysis of variance, P = 0.0000, 0.0000). BP and PR were significantly increased between 1 and 30 minutes after actual smoking as compared with control data, while IOP showed no significant change at any time of measurement. ConclusionsThese results indicated that cigarette smoking increased tissue blood velocity in the ONH and possibly in the choroid in habitual smokers.