Effects Of Chronic Smoking Research Articles

Independent association of various smoking characteristics with markers of systemic inflammation in men. Results from a representative sample of the general population (MONICA Augsburg Survey 1994/95).

Aim of the study was to investigate the association between various markers of systemic inflammation and a detailed history of smoking in a large representative sample of the general population. The effects of chronic smoking on white blood cell (WBC) count, fibrinogen, albumin, plasma viscosity (PV), and high-sensitivity C-reactive protein (CRP) were measured in 2305 men and 2211 women, age 25-74 years, participating in the third MONICA Augsburg survey 1994/95. In men, current smokers showed statistically significantly higher values for WBC count, fibrinogen, PV, and CRP, compared to never smokers, with intermediate, but only slightly increased values for ex-smokers and for occasional smokers. No consistent associations were seen with albumin. Duration of smoking was positively associated with markers of inflammation as were pack-years of smoking. Conversely, duration of abstinence from smoking was inversely related to these markers. Except for WBC count, no such associations were found in women. Data from this large representative population show strong associations between smoking and various markers of systemic inflammation in men. They also show that cessation of smoking is associated with a decreased inflammatory response, which may represent one mechanism responsible for the reduced cardiovascular risk in these subjects.

Early contrast sensitivity loss and oxidative damage in healthy heavy smokers

AbstractObjective: The purpose of this study was 1) to evaluate visual functions and the activities of antioxidant enzymes in plasma and erythrocytes in smokers in comparison with non‐smokers, 2) to evaluate the correlations between visual functions and the oxidant/antioxidant system. We hypothesized that the changes in antioxidant system and consequently lipid peroxidation depend on smoking may affect sophisticated visual tests including contrast sensitivity (CS) and pattern visual evoked potentials (PVEP)Subjects: This non‐randomised control study included 24 chronic, heavy smokers who were smoking more than 20 cigarettes per day at least for last 10 years. Sixteen age and sex‐matched, healthy, non‐smokers were taken as controls. All volunteer subjects were accumulated from the outpatient clinic. To rule out the effect of alcoholism and malnutrition, we chose young, healthy heavy smokers who maintained adequate diet and who had no alcohol consumption history.Following visual acuity and color vision tests, all subjects were applied to CS and PVEP tests. Values of CS, N75‐P100 amplitude and P100 wave latency were compared between the study and control subjects. Superoxide dismutase (SOD) and catalase (CAT) activities in plasma and erythrocytes were determined by spectrophotometer. Plasma malondialdehyde (MDA) level, as an end product of lipid peroxidation, was assessed by spectrofluorometric method.Results: CS was determined to be significantly reduced in smokers compared to non‐smokers, although central vision and PVEP responses were not affected. Erythrocyte SOD activity and plasma MDA levels were significantly increased in smokers compared to controls. There were positive correlations between plasma SOD and erythrocyte SOD; CS and erythrocyte SOD; and CS and plasma SOD.Conclusions: The results suggest the possible association between early CS loss and increase in antioxidant enzyme activities thus reflecting an increased oxidative damage due to cumulative effect of chronic smoking. Elevated concentrations of lipid peroxidation products in the plasma of smokers may directly show the increased oxidative damage in these subjects.

Effects of smoking status and smoking cessation on leptin levels.

Cigarette smoking is associated with lower body weight, and quitting smoking typically produces weight gain. An effect of chronic smoking on increasing leptin, a protein product associated with reducing weight, may help explain this influence of smoking on lowering body weight. We examined fasting serum leptin levels in male and female adult smokers (n = 52) and non-smokers (n = 12) as well as long-time ex-smokers (n = 13), with all groups similar in body mass index (BMI). Partial regression analyses controlling for BMI and, where relevant, age were used to relate leptin to indices of smoking exposure and dependence within the smokers, and with typical alcohol and caffeine intake in the entire sample. Furthermore, a subset of the smokers (n = 22) quit for at least 3 weeks, and changes in leptin and weight were prospectively assessed. Results showed no difference in mean leptin levels as a function of smoking status and no significant associations of leptin with smoking exposure variables after controlling for BMI and age. However, leptin was significantly correlated with alcohol intake (inversely) in women. In addition, smoking cessation increased leptin, the opposite change expected if leptin were responsible for weight gain, but again only in women and not in men. This leptin change remained significant after controlling for the increase in weight observed in both men and women. In conclusion, the influence of cigarette smoking on body weight does not appear to be due directly to changes in leptin levels, as there is no difference in leptin due to smoking status and leptin does not decline after cessation.

Influence of smoking and Helicobacter pylori on gastric phospholipids.

Smokers show higher rates of peptic ulcer disease (PUD) than nonsmokers, probably due to detrimental effects on the gastric mucosa. Surface-active phospholipids (SPL) are believed to play a key part in gastric cytoprotection. The aim of this study was to determine the chronic effects of smoking on the gastric SPL and to relate them to H. pylori (Hp) -induced effects. Gastric juice was aspirated in 52 patients, with normal findings at planned upper gastrointestinal endoscopy, and concentrations of seven phospholipid subclasses were analyzed. Concentrations of lysophosphatidylethanolamine (1-PE) were increased (P = 0.006) in smokers compared to nonsmokers in non-Hp-infected samples. Nonsmokers infected with Hp showed increased levels of 1-PE (P = 0.01) and phosphatidylinositol (PI) (P = 0.02) compared to subjects not infected. In human gastric juice PI seems to be the dominating PL subclass, in contrast to the composition in biopsy specimens. We also found both Hp-infected and smoking subjects to have higher concentrations of more polar phospholipid subclasses, ie, 1-PE, making the mucosa more vulnerable to acid attack as the gastric surfactant becomes less hydrophobic.

Smoking is associated with dose-related increase of intima-media thickness and endothelial dysfunction.

Cigarette smoking is firmly established as a risk factor for atherosclerosis. However, the exact mechanism causing smoking-related damage to the arterial wall and its relation to the atherosclerotic process is not known. Also unknown is the time delay between the start of smoking and the sequence of functional and morphologic changes occurring in the arterial wall caused by smoking and their interrelationship. Therefore, the aim of this study was to evaluate the acute and chronic effects of smoking on endothelium-dependent (flow-mediated) dilation (FMD) of the peripheral arteries, the effects of dose and duration of chronic smoking on intima-media thickness (IMT) of the carotid arteries, and their interrelationship. The study encompassed two groups of smokers. In group A there were 40 subjects of both sexes, who smoked on average 17.6 +/- 6.5 cigarettes per day, for 5 to 15 years (mean 8.95 +/- 4.0 years), mean age 28.1 years. Group B consisted of 42 smokers of both sexes who smoked 21.15 +/- 8.2 cigarettes/day for more than 15 years (mean 21.15 +/- 3.4 years), mean age 39.5 years. The control group consisted of 40 healthy subjects without major risk factors of atherosclerosis, mean age 29.1 years. By means of high-resolution ultrasound the brachial artery diameter was measured at rest and during reactive hyperemia (after release of a forearm tourniquet) and the flow-mediated, endothelium-dependent dilation was calculated. The IMT of the carotid arteries was determined in all subjects by use of B-mode ultrasonography. Resting blood flow in the brachial arteries was significantly less in the smokers' groups than in controls (78.8 +/- 31.9 vs 134.9 +/- 45.0 mL/min, p<0.0001). This decrease was much more evident in female than in male smokers. Female smokers also had significantly smaller brachial artery diameter at rest. In smokers the FMD of the brachial artery was reduced (11 +/- 4% vs 7 +/- 4%, p<0.004) and the mean IMT was significantly greater than in controls (0.68 +/- 0.13 vs 0.59 +/- 0.04 mm, p<0.001). Impairments of FMD and IMT increase were related to the duration and to the number of cigarettes smoked. In all subjects IMT was significantly correlated with total and LDL cholesterol, fibrinogen, lipoprotein(a) concentration, body mass index, and age of the subjects, but multivariate analysis showed that only total dose smoked and fibrinogen concentration were independently related to IMT. The results of this study show that smoking is associated with dose-related impairment of FMD and increased IMT of the carotid arteries. Impairment of FMD occurs in smokers very early and is the earliest detectable event, preceding morphologic changes of the vessel wall. Some harmful effects of smoking on the vessel wall are gender related.

Acute and Chronic Effects of Smoking on Blood Antioxidant Status

In this study, the possible effects of smoking on plasma and erythrocyte antioxidant status were investigated. For this purpose, thiobarbituric acid reagent substances (TBARS) and antioxidant potential (AOP) values were measured in both erythrocyte and plasma samples before and after five cigarettes smoked at fasting. AOP and TBARS levels were measured in non-smokers as well, to be used as a control group. We found that TBARS levels were higher in both plasma and erythrocyte samples and AOP levels lower in erythrocyte but unchanged in plasma samples from smokers as compared with non-smokers. After cigarette smoking, no meaningful changes were observed in TBARS and AOP values of plasma but both TBARS and AOP values increased in erythrocytes of the smoker group. The results suggest that chronic smoking causes peroxidation reactions in both plasma and erythrocytes, and acute smoking induces oxidation reactions in erythrocytes, even though AOP also elevates as a compensatory mechanism. In contrast to chronic ...

Inhibitory effect of smoking on event-related potentials in schizophrenic patients: Comparison with healthy subjects

1. 1. A prior study demonstrated that the P300 peak amplitude of event-related potentials increased during acute withdrawal and smoking resumption in healthy subjects. Here the authors measured the P300 components in schizophrenic patients under similar conditions and compared them to normal controls. 2. 2. The P300 amplitude and area negatively correlated with the daily nicotine intake. 3. 3. The P300 amplitude and area were reduced by smoking resumption following overnight abstinence. 4. 4. The P300 components did not correlate significantly with the Brief Psychiatric Rating Scale or the equivalent neuroleptic dosage. 5. 5. The inhibitory effect of smoking was prevented by pretreatment with nicotine gum. 6. 6. In schizophrenics and healthy subjects, the chronic effects of smoking were similar. However, acute abstinence and smoking resumption decreased the P300 amplitude in schizophrenic patients but increased the amplitude in normal subjects. These results suggest that nicotine differentially affects arousal in schizophrenic patients and healthy subjects.

Measurement of the time course of peripheral vasoactivity: results in cigarette smokers

The brachial artery response to flow was assessed non-invasively by ultrasonic measurement of arterial diameter before and 1 min after 5 min of cuff-induced ischemia. It was hypothesized that continuous measurement of arterial diameter and flow velocity would provide a more complete and accurate evaluation of the response to change in blood flow. Therefore, a system to provide this data was developed and its utility in exploring the acute and chronic effects of smoking on arterial function was demonstrated. Brachial artery diameter and flow velocity were measured before, during and for at least 3 min after 5-min of forearm cuff occlusion. Measurements were acquired from 12 habitual smokers (mean 18.3 pack years), after at least 2 h (mean 6.5 h) without smoking (‘pre-cigarette’) and immediately after smoking one cigarette (‘post-cigarette’), as well as from 12 age- and sex-matched lifelong non-smokers. The slope of brachial artery diameter versus time during the occlusion period and the maximum dilation after cuff release relative to the pre-occlusion diameter were significantly decreased in pre-cigarette smokers compared with non-smokers ( P<0.0001 for both comparisons). Importantly, the absolute arterial dilation during the period of increased flow (i.e. reactive hyperemia) was equal for the pre-cigarette smokers and non-smokers (0.31±0.03 vs. 0.32±0.04 mm, respectively). Immediately after smoking, the flow response parameters in chronic smokers changed toward non-smoker values ( P<0.001 for post-cigarette vs. pre-cigarette comparisons of the diameter slope during occlusion and the maximum dilation after cuff release relative to pre-occlusion diameter). Thus, continuous diameter measurements in smokers who refrained from smoking demonstrated abnormal constriction of the brachial artery during the low flow period of cuff occlusion, but normal absolute dilation during the period of increased flow. Immediately after smoking, the artery no longer constricted during occlusion. These findings demonstrate the potential value of continuous monitoring of arterial diameter and flow velocity before, during and after application of a vasoactive stimulus.

Effect of Long-term Passive Smoking on Erectile Function and Penile Nitric Oxide Synthase in the Rat

Given that smoking is a risk factor for erectile dysfunction, this study aimed to determine, in a rat model, whether long-term exposure to cigarette smoke impairs nitric oxide (NO)-dependent erectile function and reduces penile nitric oxide synthase (NOS), and if these changes are accompanied with effects on the systemic blood pressure. Adult (5 month) and old (20 month) rats were exposed to daily passive smoking for 8 wks. Three days after the conclusion of exposure, half of the animals were submitted to electrical field stimulation (EFS) of the cavernosal nerve and the maximum intracavernosal pressure (MIP) and mean arterial pressure (MAP) were determined and expressed as mm. Hg. On the other half of the animals, NOS activity in the penile cytosol was measured by the arginine/citrulline assay, and neuronal NOS (nNOS) and endothelial NOS (eNOS) contents were estimated by western blot and densitometry. When compared to controls, the smoking rats had a higher MAP in both the adult (115 vs 162) and old (113 vs 140) rats, but surprisingly the MIP also increased, from 78 to 111 (adult rats) and from 59 to 83 (old rats). Smoking reduced penile NOS activity by 73% (adult rats), and 62% (old rats), and nNOS content by 43% and 50%, respectively. In contrast, eNOS was not affected. Nitrite release, in vitro, by cavernosa slices or in rat penile smooth muscle cells (RPSMC) was not inhibited by nicotine or cotinine. These results indicate that chronic smoking in the rat leads to age-independent moderate hypertension and considerable decreases in penile NOS activity and nNOS content, that are not reflected in a reduction of the erectile response to EFS or accompanied by a decrease in penile eNOS.

Evidence from a Chronobiometric Approach That Chronic Smokers, Although Normotensive, Show an Increase in Diurnal Blood Pressure

To investigate the effects of chronic smoking on the 24 h blood pressure and heart rate pattern in normotensive subjects. Twenty-five smokers and 25 age-, weight- and height-matched non-smokers, who were all clinically healthy young men, gave their informed consent to undergo non-invasive, automated, ambulatory blood pressure monitoring for 24 h. The smokers in this study consumed on average 25.4 cigarettes per day. The lifestyle of the two groups was comparable because they worked as clerks at the same company. The 24 h blood pressure and heart rate data were analysed according to chronobiological methods. Smokers were found to show a statistically significantly higher blood pressure versus non-smokers by day but not by night. Furthermore, smokers showed a slight increase in the mean level of circadian blood pressure rhythm versus non-smokers, accompanied by an amplification of one cyclic component of this periodicity. The increase in diumal blood pressure in smokers might be regarded as the haemodynamic effect of chronic smoking in normotensive subjects. Such an effect seems to be substantiated pathophysiologically by an amplitude overmodulation of one of the harmonic components which confer the circadian blood pressure rhythmicity. Because the diumal increase in blood pressure persists for two-thirds of the day-night period, one can argue that this phenomenon in normotensive smokers might be a premonitory sign of future hypertension. Apart from this, one can hypothesize that the diumal increase in blood pressure might itself be a cause of target organ damage, given its consistent within-day duration and daily repetition.

The effects of chronic smoking on the fibrinolytic potental of plasma and platelets

Department of Medicine, St John's Hospital, Livingston 1 Department of Molecular and Cell Biology, University of Aberdeen, Aberdeen, UK

Effects of alcohol intake on resting energy expenditure in young women social drinkers

This investigation evaluated the effects of alcohol consumption, controlled for the energy in alcohol and chronic effects of smoking, on resting energy expenditure (REE) in college-aged social drinkers. Sixteen women who both smoked and drank alcohol were administered, on 4 separate days in a counterbalanced order, 1) cigarettes alone, 2) alcohol alone, 3) alcohol plus cigarettes, or 4) cigarettes with an energetic control. Each session consisted of a 25-min REE baseline, treatment in a randomly assigned order, and a 105-min assessment of REE. Analysis indicated that alcohol significantly (P < 0.05) increased REE for up to 95 min after ingestion [increases of 29.6-68.4 kJ (124-287 kcal)/24 h], increases that could not be accounted for by the energy content of the drink alone. Smoking and alcohol together also raised REE above baseline but not more than alcohol alone. It was concluded that alcohol intake raises REE, potentially explaining why alcohol interferes with energy utilization. Potential implications for alcohol intake, nutrition, and weight loss are presented.

Effect of Chronic Smoking on Digital Blood Flow: A Preliminary Report

A study of digital blood flow was carried out using a "mercury-in-silastic" strain gauge in 50 individuals. Forty heavy smokers (25 asymptomatic chronic heavy smokers and 15 smokers with overt thromboangiitis obliterans—TAO) were studied. Ten individuals who had never smoked served as controls. Chronic heavy, long-term smoking causes signifi cant reduction in digital blood flow. A further reduction occurs in those with overt symptoms of TAO. Monitoring of digital blood flow could provide a good screening test for determining the status of peripheral blood flow in chronic smokers.

Effect of chronic smoking on endothelium-dependent vascular relaxation in humans.

1. Cigarette smoking is one of the major risk factors for the development of atherosclerosis. It is not clear, however, whether chronic cigarette smoking impairs the normal physiological function of the endothelium before the development of morphological vascular lesions. To test this, we investigated endothelium-dependent vascular relaxation in young habitual smoking subjects. 2. In 11 non-smokers and 10 habitual smokers we measured the changes in bilateral forearm blood flow, arterial blood pressure and forearm vascular resistance (ratio between mean arterial blood pressure and forearm blood flow) during three interventions: post-occlusive forearm hyperaemia, intrabrachial infusion of methacholine which causes vasodilatation by stimulating the release of endothelium-dependent relaxing factor, and intrabrachial infusion of sodium nitroprusside which causes vasodilatation independently from the endothelium by a direct effect on the vascular smooth muscle wall. 3. During infusion of the highest dose of methacholine, forearm vascular resistance decreased by 91.7 +/- 1.4% in the smokers and by 89.9 +/- 1.8% in the non-smokers. During infusion of sodium nitroprusside, forearm vascular resistance decreased by 80.0 +/- 3.8% in the smokers as compared with 80.7 +/- 6.1% in the non-smokers. There was no difference in basal forearm vascular resistance or in post-ischaemic reactive hyperaemia between smokers and non-smokers. Thus, vasodilatation induced by both methacholine and sodium nitroprusside was not significantly different between smokers and non-smokers. 4. We conclude that in young habitual cigarette smokers the endothelium-dependent vasodilation in the forearm seems to be preserved, suggesting that habitual smoking does not result in permanent endothelial dysfunction in the human forearm.

Effects of tobacco smoking on caloric intake.

Reduced body weight due to smoking may be an important factor inhibiting smoking cessation and promoting relapse after cessation in some smokers. It is popularly believed that smoking decreases body weight by suppressing appetite. However, cross-sectional studies show that, despite their lower body weights, smokers do not eat less than non-smokers or ex-smokers and, in fact, tend to eat slightly more. Similarly, laboratory studies show no acute effects of smoking or nicotine intake via other means on caloric intake in smokers, although intake of non-smokers may be reduced after nicotine. In contrast, longitudinal studies show that eating consistently increases in the first weeks after stopping smoking, but may recede to pre-cessation levels with longer-term abstinence, while resumption of smoking after cessation is accompanied by a reduction in eating. A similar pattern of results is seen for self-reported hunger and some, but not all, constituents of diet. Thus, there appear to be no acute or chronic effects of smoking on eating in smokers maintaining regular smoking, but changes in eating are observed concomitant with changes in smoking status (i.e. cessation or relapse). Although tolerance to anorectic effects of nicotine is one potential explanation, these findings may be more parsimoniously explained by viewing changes in eating due to smoking as secondary to an alteration in the set point around which body weight is regulated. According to this notion, cessation is accompanied by increased eating only until a new, higher body weight set point is reached, while relapse (and perhaps initiation of smoking) decreases eating only until a lower set point is reached. Implications of these findings and a set point explanation for them are discussed.

The acute effect of smoking on platelet and endothelial release reaction is suppressed in chronic smokers

Whilst increased plasma β-thromboglobulin (BTG), platelet factor 4 and thrombospondin levels are regarded as reflecting the release reaction of platelets, tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) levels represent endothelial release reaction and/or damage. In this study including 12 smokers and 9 nonsmokers, we investigated the acute and chronic effect of smoking on these parameters and antithrombin III, protein S and fibrinogen, as well. Nonsmokers were found to have somewhat higher plasma levels of βTG, t-PA and PAI-1 than chronic smokers, and 30 minutes after smoking two cigarettes, these levels and protein S levels of nonsmokers showed more prominent increases than of chronic smokers. It is speculated that chronic exposure to cigarette smoke may cause “exhaustion” or “receptor down-regulation” of platelets and endothelial cells, resulting with diminished release reaction of platelets and endothelium in response to acute smoking.

Twenty-four-hour urinary-free cortisol in premenopausal cigarette smokers and nonsmokers

Cigarette smoking has been reported to produce acute increases in plasma ACTH and cortisol, but the effect of chronic smoking on integrated adrenal steroid production has not been studied. The effects of chronic smoking on 24-hour urinary-free cortisol, 11-deoxycortisol, DHEAS, and 17-keto-steroids were studied in 10 premenopausal smokers, and their results were compared with 15 premenopausal nonsmokers. The 24-hour excretion of urinary-free cortisol (85.0 +/- 40.8 nmol/d in smokers versus 81.7 +/- 49.7 nmol/d in nonsmokers), 11-deoxycortisol (259 +/- 170 nmol/d in smokers versus 222 +/- 147 nmol/d in nonsmokers), DHEAS (3,140 +/- 2,909 nmol/d in smokers versus 2,890 +/- 1,960 nmol/d in nonsmokers), and 17-ketosteroids (17.4 +/- 8.3 mumol/d in smokers versus 23.4 +/- 19.9 mumol/d in nonsmokers) were similar in smokers and nonsmokers (all P values not significant). We conclude that chronic smoking does not result in abnormal levels of 24-hour urinary-free cortisol.

Biochemical evidence of a chronic abnormality in platelet and vascular function in healthy individuals who smoke cigarettes.

Cigarette smoking is associated with increased mortality from cardiovascular disease that declines after cessation. This study extends the evidence regarding the effects of chronic smoking on platelets and the vessel wall in vivo. Excretion of a major urinary thromboxane metabolite, 2,3-dinor-thromboxane B2, is significantly (p less than .01) elevated in apparently healthy chronic smokers (20 cigarettes daily) compared with that in nonsmoking control subjects. This difference in excretion of 2,3-dinor-thromboxane B2 was abolished by the administration of 20 mg aspirin twice daily, a dose shown to selectively inhibit platelet cyclooxygenase. After aspirin, the return of the excretion of 2,3-dinor-thromboxane B2 to pretreatment levels paralleled the recovery of platelet cyclooxygenase. These findings indicate that excessive thromboxane A2 generation in chronic smokers predominantly derives from platelets. The urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha also is increased during chronic cigarette smoking, as is the case with other diseases associated with accelerated interaction of platelets with the vessel wall. We have found evidence of platelet and vascular dysfunction in vivo in chronic cigarette smokers before the manifestation of overt cardiovascular disease. The results would also be consistent with the hypothesis that in chronic smokers, the platelet defect is largely reflective of smoking-induced vascular injury.

Serum angiotensin converting enzyme activity in ex-smokers

A low activity of angiotensin converting enzyme (ACE) has been reported in people who smoke. To determine whether this low ACE activity would be reversible on cessation of smoking, we measured serum ACE activity in 107 healthy male volunteers. They included 27 active cigarette smokers, 28 non-smokers, 24 ex-smokers who had stopped smoking for less than 10 yr, and 28 ex-smokers who had stopped smoking for more than 10 yr. The mean value (±SD) of serum ACE in those who had stopped smoking for more than 10 yr was comparable to that of non-smokers: 23.2 ± 5.1 and 23.5 ± 4.5, respectively. ACE activity in smokers and the ex-smokers who had stopped smoking for less than 10 yr was significantly lower (17.8 ± 4.5 and 17.8 ± 3.9, respectively) than values obtained in non-smokers and the group who had not smoked for more than 10 yr ( p < 0.001). These findings suggest that the effect of chronic smoking on the serum ACE activity may be reversible.

Effects of smoking on regional cerebral blood flow in cerebral vascular disease patients and normal subjects.

The chronic effect of smoking on the regional cerebral blood flow (r-CBF) was studied by 133-Xenon inhalation method and described with the Initial Slope Index (ISI). Fifty-two patients as the control group who had no abnormality neurologically or with CT scan, 32 patients with old cerebral infarction and 20 patients with old cerebral hemorrhage were introduced to the present study, and these patients were divided into smokers and non-smokers in each group. Those whose smoking index of 200 or more [(number of cigarettes/day) X (years of smoking history) greater than or equal to 200] were designated as smokers. ISI values were decreased significantly in smokers than non-smokers in all groups. Mean ISI value of unaffected hemisphere in smokers decreased by 16% in the infarction group and 22% in the hemorrhage group comparing to the non-smokers', respectively. In the control group, mean ISI value of right hemisphere decreased by 15% and left 14% in smokers compared to the non-smokers. The r-CBF values in 44 of the 47 smokers were found to be lower than the expected age matched values in non-smokers. Serum high density lipoprotein cholesterol value in smokers was significantly lower than that in non-smokers. We demonstrated preliminarily that the smoking chronically reduced the r-CBF. Advanced atherosclerosis associated with the smoker was suggested to affect the CBF.