ernia and diabetes fnellitus (1). and atheroscleroservations the prevalence of smoking and mortality from coromry heart disease have declined, but 25% of all ~~~~~~v~s~~lar deaths in the developed countries are still attributable to cigarette smoking (3). Even in countries where the incidence of coronary heart disease is relatively low, smoking shows From the Departmentof Pharmacology,Divisionof ClinicalPharmacologyand Departmentsof Biophysicsand Physiology,CardiovascularResearch Institute Maastricht,University of Limbuq, Maastricht,The Netherlands. Manuscriptreceived March29, 1993;revised manuscriptreceived.iarne 1% I Dr. M. J. F. Kool, Deparwnt of Pharmacology, University of Limburg, P. 0. Box 616, 6209 MD Maastricht,The Netherlands. 81993 by the AmericanColtegeof Cardiology T 1. DemographicDatafor Smokersand Nonsmokers Gender Ageiyr) Weight (kg) He&%(cm) BU (m3, Smokers (n = 14) Nonsmokers (n = 14) 9Ml5F 37 (25-W 73 (55-88) 175(158-186) 1.9(M-2.1) 9M;SF 37(w-541 72 (52-931 174(161-183) 1.9(1.6-2.0) Vahwsin [email protected] = body surfacearea, calculated accord&~to tie fomwh of Ih Boisand Du Bois (14). the left arm. Pulse pressure (AP) was ~efi~cd as ~y~to~~c minus diastolic blood pressure. bit& smokers (study 1). In addition, these!v were compared with those in ~n~~~~~~~ subjects (study 2). arm at heart level. The whole arm was deiced in an incubator to keep c~vironm~ntal nstant (28°C).In addition, the skin temperay a skin electrode thermomrature was similar before and E&C common carotid bl every mmute. In addition, cardiac flowwere determined before and strain gauge, represent total (cutaneous and muscle) forearm blood flow. Hand circulation was eliminated by inflating a wrist cuff to suprasystolic pressure (220mm Hg) for 4 min. Figure 1. The short-term effec’ of smokingon vessel wall properties of large arteries before (open bsrs) and after (solid bars) smokingone cigarette. Data are mean value -1SEM. *p c Q.05,**p < 0.01(diqerence between period before and after smoking).BA = brachialartery; = complhce coeficient; ::* = common carotid artery; D = diameter; DC = distensibility coefkient. 6 KWL E’K’AL. I SMOKING AND AK’I’ERIAL WALL PROPERTIES 3. HemodynamicIMa for Smokers and Nonsmokers Smokers bighsic s&33, At low doses Nonsmokers of smoking can be explained by the ~~cot~~e~~~d~cc~ sympathetic activation. Nicotine induces t e release of both epinephrine and ~orep~~e~bri~~, thetic nerve activity has been ), the increase in plas cts stimulation of the adre peripheral mecba~~sms(e nephrine clearance) (18)+The net dependlenton the mixed nephrine at the d~er~~t it causes medulla awd an d stimulation or direct in these studies the increment in is lower than the incrczss in heart se short-term hemodynamiceffects After a 4-h noasmoking period, heart rate at rest was higher in habitual smokers than in nons~~lokers.This differcace could not be explained lay differences in physical activity level in the two groups because, on average, smokers and nonsmokers beloved the same daily work and s activatorswere comparabk. In previous studies, smokers (26)the heart rate has been persistently could to be elevated of withdrawal phenomenon. rs in our study was not different from that in nonsmokers. Other studies have been inconsistent with regard to blood pressure in habitual smokers. Overall (X,27), casual as well as ambulatory blood pressure values in habitual smokers have 2. 3. om mtional vitsnlstatistics. Lancet tW;J39: 1268-78. Kiyohara Y, Ueda K, Fujishima M. Smoking and sar&vascu?x discasf: in the general population in Japan. J Hypertens I%%;8 Suppl %W-15. Glantz SA, Rarmley VW. Passive sm0,king and heart disease. Epiderniology, physiology and biochemistry. Circulation 19%;83: 1-12. Cruickshank JM, Neil-Dwyer G, Dorrance DE, Hayes Y, Pate1 S. Acuk effects of smoking on blood pressure and cerebral blood flow. J Hypertens 19&9;3:443-9. 7. LepPntalo M, Lassila 8. Smoking and occlusive arterial disease. Sug %991;157:83-7. 8. Bijhler FR, Vesanen K. Walters JT. Ii P. Impact of smoking on heart attacks, strokes, blood pressure co I, drug dO!X, iKId C$ldily Of life aspects in the International Ptospeclive Primary Brevcntiori Study in Hypcncasioa, Am Heart J 19Xi;l15:2#2-7. 9. DOllWy C, !%Wi~ii~ t?F. TktZ lrial: the smoking pahnl. Am 10. Bcnowitz NL. Pharmacologica addiction. N En@ J Med 1988;319:1318-30. II. function and kemostasis (20,34,35). In addition, according to the current view of atherosclerotic disease, plaque ruptun is an important feature. Pt has been demonstrated that most of the acute coronary syndromes are due to the disruption of small, nonstenotic plaques (36). These small plaques are generally not detected with the present diagnostic techniques and might already be present in young smokers (36). Increased arterial wall stiffness, increased blood pressure ad a bigher heart rate are short-term effects of smdhg that enhance the load on the site. sf ~t~~~osc~e~ot~~ vessel wall. In addition, at t plaques, the distribution of circu rential and tensile stress is altered, which might further increase the load at the plaque (37).The smoking-induced increased load at the atherosclerotic plaque may induce plaque rupture and lead to acute ischemic events. 12. 13. 14. 15. 16. Van Bortel LM. 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