Abstract-Environmental tobacco smoke (ETS) acutely affects peripheral and coronary vascular tone. Whether ETS exerts specific deleterious effects on aortic wave reflection through nicotine exposure, whether they persist after ETS cessation, and whether the smoke environment impairs microvascular function and increases asymmetrical dimethyl-arginine levels are not known. We tested these hypotheses in a randomized, crossover study design in 11 healthy male nonsmokers. The effects of 1 hour of exposure to ETS, as compared with a nontobacco smoke and normal air, on augmentation index corrected for heart rate and skin microvascular hyperemia to local heating were examined. Augmentation index increased both during (Pϭ0.01) and after (PϽ0.01) the ETS session but remained unchanged in the nontobacco smoke session when compared with normal air. Nicotine levels after the exposure were related to the peak rise in augmentation index (rϭ0.84; PϽ0.01), denoting a predominant role of nicotine in ETS vascular effects. This was confirmed in a second set of experiments (nϭ14), where the sublingual administration of nicotine was associated with an acute impairment in wave reflection as compared with placebo (Pϭ0.001). Both ETS and nontobacco smokes increased plasma asymmetrical dimethyl-arginine levels (PϽ0.001), but only ETS reduced the late rise in skin blood flow in response to heating (Pϭ0.03). In conclusion, passive smoking specifically increases aortic wave reflection through a nicotine-dependent pathway and impairs microvascular function, even after the end of the exposure. However, both tobacco and nontobacco passive smoking inhalation increase plasma asymmetrical dimethyl-arginine levels. Key Words: passive smoking Ⅲ nicotine Ⅲ endothelium Ⅲ wave reflection Ⅲ nitric oxide E xposure to environmental tobacco smoke (ETS) has been recognized recently as a strong contributor to cardiovascular mortality, accounting for Ͼ50 000 deaths annually in the United States. 1 In recent years, extensive research has elucidated many aspects of the long-term ETS-related adverse effects on the cardiovascular system. 1 However, the use of normal air inhalation as a control limits the interpretation of the physiopathological processes underlying the acute cardiovascular toxicity of ETS. [2][3][4] Whether lung irritation and/or the stress provoked by smoke inhalation generate a nonspecific cardiovascular reaction 5 and whether this can explain the effect of ETS 2-4 are not known. We, therefore, decided to test the hypothesis that the vascular effects of ETS cannot simply be ascribed to a nonspecific reaction to smoke. This would provide further clear-cut evidence that ETS exerts specific deleterious cardiovascular effects beyond those of smoke pollution.To further prove the specificity of the toxic effects of ETS, our second new hypothesis was that the deleterious vascular effects of ETS would be related to the rise in plasma nicotine levels. The above-mentioned studies 2-4 did not determine plasma nicotine. The role of nicotine in the changes ...

The effect of endogenous and exogenously administered oestrogens, androgens and progesterone on plasma and urinary uric acid and uric acid clearance was studied in a total of 65 healthy volunteers, including normal menstruating and post-menopausal women, girls with primary amenorrhoea and adult male subjects. A serial study throughout a full cycle in 3 women showed an inverse relationship between plasma uric acid levels and endogenous oestrogens. Administration of conjugated and synthetic oestrogens produced a fall in plasma uric acid concentration through a uricosuric effect in most subjects of both sexes. Testosterone propionate caused a definite increase in plasma uric acid levels in post-menopausal women while endogenous testosterone changes due to Leydig cell stimulation produced no definite effect in male subjects. Administration of a progesterone preparation produced an effect similar to that of oestrogens in post-menopausal women. The evidence presented here supports the view that sex steroids play a significant part in uric acid regulation in biological fluids of both sexes.It has been well established that uric acid (UA) concentration in the plasma of healthy subjects is related to age and sex and that in women of reproductive age plasma uric acid (PUA) levels are markedly lower than those of adult men of comparable age (Mikkelsen et al. 1965). The underlying cause for these

These results suggest that decreased aerobic exercise capacity after intake of beta-blockers is accompanied by decreased ventilation at any metabolic rate. However, this occurs without detectable change in the sympathetic nervous system tone or in metabo- or chemosensitivity and is therefore probably of hemodynamic origin.

The exposure to lower environmental temperatures is related to impaired hemodynamics not only to the periphery but also to the aorta. In men, PM10 air-pollution levels are associated with heightened amplitude of the reflection wave leading to significant alterations in central-pulse pressure.

1. Nicotine is a well studied pleiotropic agent which occurs naturally in tobacco smoke and has been largely accused for many of the adverse effects of smoking on the cardiovascular system, including autonomic imbalance, endothelial dysfunction and coronary blood flow dysregulation. 2. The acute sympathoexcitatory effects of smoking on the cardiovascular system are partially mediated by catecholamine release, muscle sympathetic nerve excitation and peripheral chemoreceptor sensitivity increase, consecutive to nicotinic receptor stimulation in the autonomic nervous system. 3. Recent animal data suggest that nicotine promotes the oxidative and inflammatory stress to the endothelium and induces pathological angiogenesis, leading to the progression of the atherosclerotic lesions. 4. Nicotine increases myocardial work without impairing the physiological coronary vasodilatation. Consequently, nicotine per se cannot explain the sudden reduction in coronary flow reserve after exposure to both active and passive smoking. 5. Nicotine's biological effects are characterized by a rapid onset of tolerance, which can explain why nicotine administration does not elicit acute coronary and chemoreflex side-effect in smokers.

The Microlife WatchBP Home device for self home blood pressure measurement fulfills all the validation criteria of the International Protocol and can, therefore, be recommended for clinical use in the adult population.

1. Recently, we have demonstrated that cigarette smoke exposure proportionally increases plasma nicotine levels and arterial wave reflection to the aorta. However, the exact contribution of nicotine to the smoke-induced enhancement of wave reflection and the potential underlying mechanisms have not been fully investigated. 2. The present study was a prospective study in 15 healthy male non-smokers. All received a placebo and a 2 mg nicotine tablet, according to a randomized double-blind cross-over study design. Each subject underwent repeated measurements at baseline and for 1 h after nicotine or placebo intake, using carotid-femoral pulse wave velocity (PWV) to assess arterial compliance. Concurrently, aortic pressures and the augmentation index were evaluated using applanation tonometry. 3. Plasma nicotine concentrations achieved 1 h after intake of the nicotine tablet reached comparable levels to those achieved after 1 h exposure to passive smoke (3.6 +/- 0.4 vs 3.2 +/- 0.4 ng/mL, respectively; P = 0.4). 4. Nicotine enhanced arterial wave reflection to the aorta, as assessed by the augmentation index corrected for heart rate (4.2 +/- 1.3 vs-0.7 +/- 0.8% with placebo; P = 0.001). In addition, a progressive increase in carotid-femoral PWV was noted after nicotine administration (0.3 +/- 0.1 vs-0.02 +/- 0.1 m/s with placebo; P = 0.04). This remained significant even after adjustment for changes in mean blood pressure and heart rate (P = 0.01). 5. Plasma nicotine concentrations comparable to those achieved after exposure to passive smoke enhance arterial wave reflection to the aorta. This is accompanied by an increase in carotid-femoral PWV, denoting a deterioration of arterial compliance by nicotine.

Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post-handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O 2 in N 2 , chemoreflex activation without metaboreflex activation); and (4) post-handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (−42 ± 7% muscle sympathetic nerve activity (MSNA) mmHg −1 ), sympathetic baroreflex sensitivity did not change during normoxic post-exercise ischaemia (PEI; −53 ± 9% MSNA mmHg −1 , P = 0.5) and increased during resting hypoxia (−68 ± 5% MSNA mmHg −1 , P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (−35 ± 6% MSNA mmHg −1 , P < 0.001 versus hypoxia without exercise; P = 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 ± 1.7 ms mmHg −1 ), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 ± 1.3 ms mmHg −1 , P = 0.09), but decreased during resting hypoxia (7.3 ± 0.8 ms mmHg −1 , P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 ± 1 ms mmHg −1 , P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia.