Effects of beta-blockers on hemodynamics of the forearm after tobacco stimulation

Girerd, X.; Brunel, P.; Laurent, S.; Pannier, B.; Isnard, R.; Safar, M.

Archives des Maladies du Coeur et des Vaisseaux 81(Special Issue): 133-136

1988


ISSN/ISBN: 0003-9683
PMID: 2903727
Document Number: 318375
In mild hypertension, a betablocker treatment could reduce cardiovascular events. But in smoking men the benefit disappears and this interaction is unexplained. In 6 healthy non smoking men, we studied the effects of acute oral administration of propranolol (80 mg) pindolol (15 mg) and placebo after cigarette smoking (CS) (two cigarettes within 10 minutes). In a double blind cross over randomized study, arterial pressure and heart rate (HR) were recorded within 20 minutes after CS. Brachial artery diameter (D), Local vascular Resistance (RL), Local arterial Compliance (CL) and pulse wave velocity (VOP) were determined non invasively (using a pulsed doppler system) before and 20 mn after CS. Under placebo, mean arterial pressure (PAM), HR and RL increased significantly after CS (+9.2 +/- 3 mmHg, +4.5 +/- 3 b/mn and +36 +/- 14 per cent, respectively). These modifications were not different after propranolol, pindolol or placebo (ANOVA). Arterial distensibility (CL) was decreased after CS and this alteration was not prevented by beta-blockers. Brachial artery diameter was not modified after CS. Our results demonstrate that acute treatment with non selective beta-blockers with or without sympathomimetic intrinsic activity does not prevent haemodynamic modifications induced by cigarette smoking.

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