Effects of acute smoking on the hemostatic system in humans

A. M. Vicari, A. Margonato, A. Macagni, R. Luoni, M. P. Seveso, G. Vicedomini, G. Pozza

Research output: Contribution to journalArticle

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Abstract

Habitual smoking is one of the best established risk factors for cardiovascular disease. The pathogenesis of smoke-induced damage is not so well clarified, but it probably includes - among some other aspects - an activation of the hemostatic system. Recently it has been shown that smoking a single cigarette can significantly decrease the coronary blood flow in coronary patients as well as in normal subjects. We tested the hypothesis that the acute effects of smoke are mediated by the hemostatic system. Seven healthy male volunteers, aged 20-40 years (mean 32 ± 6 years), entered the study. All were habitual smokers, but had abstained from smoking in the 12 hours preceding the test. After lying in absolute rest for about 30 minutes, each subject smoked a cigarette containing 1.2 mg of nicotine. Immediately before and after smoking, blood was drawn by clear venipuncture for the evaluation of the following hemostatic variables: collagen-induced platelet aggregation by the method of Born; thromboxane B2 (TxB2) production by platelets stimulated with collagen, radioimmunoassay (RIA); plasma beta thromboglobulin (TG) (RIA); plasma fibrinopeptide A (FPA) (RIA); plasma fibrinolytic activity in the euglobulin fraction (NEF) (fibrin plate method). The following results, respectively before and after smoking, were observed: collagen-induced platelet aggregation 55 ± 3 vs. 57 ± 6%; TxB2 100.5 ± 5.9 vs. 90.3 ± 9.0 ng/108 platelets; plasma beta-TG 20.8 ± 2.2 vs. 19.2 ± 2.3 ng/ml; plasma FPA 2.3 ± 0.3 vs. 2.2 ± 0.1 ng/ml; NEF, lysis diameter 16.8 ± 1.6 vs. 16.7 ± 1.7 mm; NEF + C1 inhibitor lysis diameter 8.8 ± 0.7 vs. 9.1 ± 0.7. None of these variables was significantly changed after smoking. We conclude that acute smoking does not induce a prothrombotic state.

Original languageEnglish
Pages (from-to)538-540
Number of pages3
JournalClinical Cardiology
Volume11
Issue number8
Publication statusPublished - 1988

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Hemostatics
Smoking
Fibrinopeptide A
beta-Thromboglobulin
Radioimmunoassay
Thromboxane B2
Collagen
Platelet Aggregation
Smoke
Tobacco Products
Blood Platelets
Serum Globulins
Phlebotomy
Fibrin
Nicotine
Healthy Volunteers
Cardiovascular Diseases

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Vicari, A. M., Margonato, A., Macagni, A., Luoni, R., Seveso, M. P., Vicedomini, G., & Pozza, G. (1988). Effects of acute smoking on the hemostatic system in humans. Clinical Cardiology, 11(8), 538-540.

Effects of acute smoking on the hemostatic system in humans. / Vicari, A. M.; Margonato, A.; Macagni, A.; Luoni, R.; Seveso, M. P.; Vicedomini, G.; Pozza, G.

In: Clinical Cardiology, Vol. 11, No. 8, 1988, p. 538-540.

Research output: Contribution to journalArticle

Vicari, AM, Margonato, A, Macagni, A, Luoni, R, Seveso, MP, Vicedomini, G & Pozza, G 1988, 'Effects of acute smoking on the hemostatic system in humans', Clinical Cardiology, vol. 11, no. 8, pp. 538-540.
Vicari AM, Margonato A, Macagni A, Luoni R, Seveso MP, Vicedomini G et al. Effects of acute smoking on the hemostatic system in humans. Clinical Cardiology. 1988;11(8):538-540.
Vicari, A. M. ; Margonato, A. ; Macagni, A. ; Luoni, R. ; Seveso, M. P. ; Vicedomini, G. ; Pozza, G. / Effects of acute smoking on the hemostatic system in humans. In: Clinical Cardiology. 1988 ; Vol. 11, No. 8. pp. 538-540.
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abstract = "Habitual smoking is one of the best established risk factors for cardiovascular disease. The pathogenesis of smoke-induced damage is not so well clarified, but it probably includes - among some other aspects - an activation of the hemostatic system. Recently it has been shown that smoking a single cigarette can significantly decrease the coronary blood flow in coronary patients as well as in normal subjects. We tested the hypothesis that the acute effects of smoke are mediated by the hemostatic system. Seven healthy male volunteers, aged 20-40 years (mean 32 ± 6 years), entered the study. All were habitual smokers, but had abstained from smoking in the 12 hours preceding the test. After lying in absolute rest for about 30 minutes, each subject smoked a cigarette containing 1.2 mg of nicotine. Immediately before and after smoking, blood was drawn by clear venipuncture for the evaluation of the following hemostatic variables: collagen-induced platelet aggregation by the method of Born; thromboxane B2 (TxB2) production by platelets stimulated with collagen, radioimmunoassay (RIA); plasma beta thromboglobulin (TG) (RIA); plasma fibrinopeptide A (FPA) (RIA); plasma fibrinolytic activity in the euglobulin fraction (NEF) (fibrin plate method). The following results, respectively before and after smoking, were observed: collagen-induced platelet aggregation 55 ± 3 vs. 57 ± 6{\%}; TxB2 100.5 ± 5.9 vs. 90.3 ± 9.0 ng/108 platelets; plasma beta-TG 20.8 ± 2.2 vs. 19.2 ± 2.3 ng/ml; plasma FPA 2.3 ± 0.3 vs. 2.2 ± 0.1 ng/ml; NEF, lysis diameter 16.8 ± 1.6 vs. 16.7 ± 1.7 mm; NEF + C1 inhibitor lysis diameter 8.8 ± 0.7 vs. 9.1 ± 0.7. None of these variables was significantly changed after smoking. We conclude that acute smoking does not induce a prothrombotic state.",
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AU - Vicedomini, G.

AU - Pozza, G.

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AB - Habitual smoking is one of the best established risk factors for cardiovascular disease. The pathogenesis of smoke-induced damage is not so well clarified, but it probably includes - among some other aspects - an activation of the hemostatic system. Recently it has been shown that smoking a single cigarette can significantly decrease the coronary blood flow in coronary patients as well as in normal subjects. We tested the hypothesis that the acute effects of smoke are mediated by the hemostatic system. Seven healthy male volunteers, aged 20-40 years (mean 32 ± 6 years), entered the study. All were habitual smokers, but had abstained from smoking in the 12 hours preceding the test. After lying in absolute rest for about 30 minutes, each subject smoked a cigarette containing 1.2 mg of nicotine. Immediately before and after smoking, blood was drawn by clear venipuncture for the evaluation of the following hemostatic variables: collagen-induced platelet aggregation by the method of Born; thromboxane B2 (TxB2) production by platelets stimulated with collagen, radioimmunoassay (RIA); plasma beta thromboglobulin (TG) (RIA); plasma fibrinopeptide A (FPA) (RIA); plasma fibrinolytic activity in the euglobulin fraction (NEF) (fibrin plate method). The following results, respectively before and after smoking, were observed: collagen-induced platelet aggregation 55 ± 3 vs. 57 ± 6%; TxB2 100.5 ± 5.9 vs. 90.3 ± 9.0 ng/108 platelets; plasma beta-TG 20.8 ± 2.2 vs. 19.2 ± 2.3 ng/ml; plasma FPA 2.3 ± 0.3 vs. 2.2 ± 0.1 ng/ml; NEF, lysis diameter 16.8 ± 1.6 vs. 16.7 ± 1.7 mm; NEF + C1 inhibitor lysis diameter 8.8 ± 0.7 vs. 9.1 ± 0.7. None of these variables was significantly changed after smoking. We conclude that acute smoking does not induce a prothrombotic state.

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