Effects Of Chronic Smoking Research Articles

Effects of chronic smoking on platelet function

Platelet function was investigated in 20 healthy cigarette smokers and 23 nonsmokers. Cigarette consumption was 1.4 ± 0.5 packs/day (mean ± SD) and the duration of smoking was 19 ± 12 years. Platelet surface activation in vitro, aggregation in vivo and in vitro, as well as the release of platelet-specific proteins in vivo were evaluated. The mean number of platelet aggregates counted on an activating surface (Formvar film) was higher in smokers (80 ± 59) than in nonsmokers (43 ± 27) (P<0.01), indicating enhanced activity following exposure to an activating surface. Smokers who were 50 years of age or older showed an enhanced platelet aggregation following an in vitro stimulation in comparison to younger smokers (105 ± 54 vs 54 ± 55 aggregates) (P<0.05). Those who smoked 20 years or more also showed enhanced aggregation in comparison to those who smoked less than 20 years (112 ± 60 vs 53 ± 45 aggregates) (P<0.02). Circulating platelets showed no significant difference among smokers and nonsmokers in the following tests: platelet aggregate ratio (0.67 ± 0.30 vs 0.86 ± 0.76), platelet count per mm3(310, 000 ± 82, 000 vs 278, 000 ± 78, 000/mmV), levels of platelet factor 4 (9.8 ± 5.2 vs 9.4 ± 5.3 ng/ml), and plasma concentrations of α-thromboglobulin (53.9 ± 23.5 vs 49.1 ± 25.5 ng/ml). The data suggest that chronic smoking primes platelets, causing them to aggregate more readily when exposed to an activating stimulus in vitro.

Cigarette smoking, gastric acid secretion, and serum pepsinogen I concentrations in duodenal ulcer patients.

Cigarette smoking has been linked with duodenal ulcer disease although the mechanism of this association is unclear. This study assessed basal gastric secretory response to acute smoking of smokers with an active duodenal ulcer; in addition the possible effects of chronic smoking on gastric secretory capacity, as expressed by pentagastrin stimulated gastric acid secretion and fasting serum pepsinogen I (PG I) concentrations, were investigated in patients with active duodenal ulcer, or non-ulcer dyspepsia. In 10 smokers with duodenal ulcer smoking four cigarettes during 40 minutes did not influence basal gastric secretion of acid and pepsin, or serum PG I and gastrin concentrations. In 136 patients with duodenal ulcer and 90 controls with non-ulcer dyspepsia, pentagastrin stimulated acid secretion and fasting serum PG I concentrations were significantly higher among habitual heavy smokers than among non-smokers. These findings suggest that in heavy smokers with duodenal ulcer acid- and pepsin-secreting cell function is not affected by acute cigarette smoking. By contrast, chronic cigarette smoking seems to be associated either with an increase of parietal- and chief-cell mass, or with an enhancement of their secretory capacity.

Effect of chronic smoking on fibrinolysis.

The aim of the study was to investigate the long-term chronic effects of smoking on the fibrinolytic enzyme system by comparing two groups of healthy male volunteers (aged 30 to 40 years). One group consisted of 15 habitual smokers who consumed 20 or more cigarettes a day; the other consisted of 15 nonsmokers. Fibrinolysis was studied at rest (baseline) and after infusion of 1-desamino-8-D-arginine vasopressin (DDAVP; 0.4 micrograms/kg body weight). Smokers had significantly lower baseline blood fibrinolytic activity as determined by the overall assays: dilute blood clot lysis (p less than or equal to 0.05) and euglobulin-fibrin plate assay (p less than or equal to 0.05). Further analysis showed that these low activities could be attributed to a lower baseline level of extrinsic tissue-type plasminogen activator (t-PA) activity (p less than or equal to 0.05) in the smokers. There were no significant differences between the groups in various fibrinolytic inhibitors or in the intrinsic fibrinolytic activation pathways. The increased levels of t-PA activity and factor VIII R:Ag in response to DDAVP were also reduced in the smokers (p less than or equal to 0.01). The relative increase (ratio of post-DDAVP activity/baseline activity) for these parameters was not significantly different for the two groups. Smokers also had significantly higher levels of the acute phase reactants, alpha 1-antitrypsin (p less than or equal to 0.02) and plasminogen (p less than or equal to 0.02) and C-reactive protein (p less than or equal to 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of smoking on regional cerebral blood flow in neurologically normal subjects.

The chronic effects of smoking on regional cerebral blood flow (CBF), and on serum lipids and lipoprotein levels in neurologically normal subjects, were studied. CBF was studied by the 133-Xenon inhalation method and gray matter flow was calculated following the method of Obrist et al. One hundred and eleven subjects, who had no abnormalities in neurological examinations nor in CT scans, were divided into two groups: smokers (37) and non-smokers (74). Those who had a smoking index (Number of cigarettes/day) X (years of smoking history) greater than 200 were designated as smokers. The mean smoking index of smokers was 760. Sixty-two of the 74 subjects in the non-smoking group had never smoked, and the mean smoking index of non-smokers was 17. In the male, CBF was significantly lower in smokers than in non-smokers (mean CBF, 12.5% lower in smokers, p less than 0.001). Increased reduction of CBF with advancing age was also observed. Compared to non-smokers, CBF in smokers was found to be significantly lower than the expected age matched value. Serum high density lipoprotein cholesterol values in smokers were significantly lower, and total cholesterol levels significantly higher than in non-smokers. We concluded that smoking chronically reduces CBF. Decrease of CBF in smokers was probably due to advanced atherosclerosis which produces vascular narrowing and raised resistance in cerebral blood vessels.

Effects of chronic smoking on testosterone metabolism in dogs

The effects of long-term cigarette smoking on androgen hydroxylases and peripheral hormones were studied in male beagles. In the testis, chronic smoking of high nicotine/tar cigarettes was associated with decreased activity of the 7α-hydroxylase active on testosterone (68% of control, P < 0.05). Testicular 6β and 16α-hydroxylases were not altered. The hepatic androgen 6β-hydroxylase activity in control animals was approximately 6 times the testis levels and was stimulated markedly by smoking. This increase ranged from 221% in the low nicotine/tar group ( P < 0.02) to 304% in the high nicotine/tar group ( P < 0.006). Serum testosterone levels were reduced to 54% of control ( P < 0.02) and prostate size to 44% ( P < 0.001) of control with heavy smoking. Serum LH levels were elevated with smoking. These results suggest that chronic cigarette smoking increased hepatic metabolism of testosterone. In addition, serum testosterone levels and prostate size decreased and LH levels increased. Whether the hepatic and the endocrine effects are causally related cannot be determined from this preliminary study.

Interaction of ozone and cigarette smoke exposure

Possible interactions of ozone and cigarette smoke exposure have been tested in 2-hr chamber exposures of 26 male and 6 female subjects, all of whom were habitual smokers. Treatment conditions were air alone, air + cigarette smoking, ozone alone, and ozone + cigarette smoking. Ozone levels were increased progressively over four trials (0.37 ppm, 0.75 ppm, 0.50 ppm + intermittent exercise, and 0.75 ppm + intermittent exercise); exercise (50 W for 15 min alternating with 15-min rest) was intended to increase ventilation by a factor of 2.5. Ozone exposure reduced the carbon monoxide intake normally seen with smoking, as judged from smaller increments of blood carboxyhemoglobin readings. Ozone exposure alone gave rise to a decrease of lung function (forced vital capacity (VC), 1-sec forced expiratory volume, and maximum flow rates at 25 and 50% of VC), but the onset was slower and the response less dramatic than previously seen in nonsmokers, suggesting that the chronic effect of smoking may be to delay bronchial irritation by ozone. Smoking increased heart rate both at rest and during exercise, but this response was not materially influenced by simultaneous ozone exposure. It is concluded that over an acute 2-hr exposure, there is no appreciable interaction between cigarette smoking and responses to ozone.

Effects of smoking on dynamic compliance and respiratory resistance.

Acute and chronic effects of smoking were studied in 68 healthy men. Current smokers, exsmokers, and nonsmokers had significantly different maximum expiratory flow rates at low lung volume (V max 25) confirming that smoking chronically impairs small airways function. After smoking one cigarette, respiratory system resistance was increased in all subjects suggesting large airways constriction. Frequency dependence of compliance (FDC) was increased after smoking one cigarette in those subjects who had little baseline FDC regardless of smoking history; these changes were partially reversed by inhalation of metaproterenol. These findings suggest that smoking narrows large airways in all subjects and also small airways in those subjects without small airways disease.

Effects of chronic tobacco smoking on the coronary circulation

The effects of chronic smoking on the coronary circulation were studied by evaluating the coronary vascular reserve in 12 chronic smokers (group 1) and 10 nonsmokers (group 2). All patients were referred to cardiac catheterization for evaluation of chest pain and were found to have normal coronary and left ventricular angiograms. Coronary vascular reserve was measured by analyzing the hyperemic response to selective coronary injection of contrast agent. There was no statistically significant difference between groups 1 and 2 with regard to age, baseline electrocardiogram or response to treadmill or thallium-201 exercise tests. The mean coronary reserve (+/- standard deviation) was 74.1 +/- 20.1% in the smokers versus 117.1 +/- 45.1% in the nonsmokers (p less than 0.02). In patients who smoked 1 pack a day or less and in those who smoked more than 1 pack a day, the mean coronary reserve was 89.5 and 64.9%, respectively (p less than 0.05). Additionally, of 20 patients followed up for an average of 20 months, 7 of 10 smokers and 1 of 10 nonsmokers continued to have chest pain (p less than 0.03). The cause for the chest pain has not been established in these patients. These results suggest that coronary vascular reserve is significantly less in chronic smokers than in nonsmokers, and that this decrease is more pronounced in heavy smokers.

Chronic Effect of Smoking on Platelet Count and “Platelet Adhesiveness” in Presumably Healthy Middle-Aged Men

In 386 men aged 40-49 years the number of platelets was related to differences in smoking habits. "Platelet adhesiveness" (retention) was estimated by a glass bead filter method in 376 of these men. The estimation of "adhesiveness" was performed in native blood without anticoagulants at least 12 hr after the last cigarette smoked. A small but statistically highly significant increase in platelet count, in number of "adhesive platelets" and percentage of "adhesive platelets" was found in smokers as compared with non-smokers, the highest values being found in the heaviest smokers and vice versa. Such smoking-related changes in platelet count and reactiveness might unfavourably influence the tendency towards coronary thrombosis, and might in part explain the deleterious effects of smoking on coronary heart disease morbidity and mortality.

Chronic smoking in an animal model: Effects on clotting and fibrinolysis

The effects of chronic smoking upon fibrinogen turnover and other clotting parameters, were studied prospectively in an animal model maintained on a chronic program for a period of 18 months. The animal received the equivalent on a weight basis of 1 1 2 packs of cigarettes daily, smoked by a human subject with the weight of 70 kg. The obtained results suggested significant enhancement of the coagulation mechanism in the smoking animals developing over the period of observation particularly when combined with high lipid diet.

Chronic effect of smoking upn pulmonary distribution of ventilation in healthy males.

Chronic effect of smoking upn pulmonary distribution of ventilation in healthy males.