HEMODYNAMIC AND REGIONAL BLOOD-FLOW RESPONSES TO NICOTINE AT REST ANDDURING EXERCISE

We hypothesized that nicotine compromises cardiovascular responses to dynamic exercise. Hemodynamic variables were measured in conscious min iswine before and at 2 min of nicotine infusion (20 mu g . kg(-1). min (-1); i.a.; N = 6) during resting conditions. Mean arterial pressure e levations (MAP; 14%) and plasma nicotine concentrations (49 +/- 7 ng . ml(-1)) were similar to those elicited by cigarette smoking in humans . In addition, nicotine increased systemic vascular resistance (SVR; 5 6%), the heart rate X systolic blood pressure product (RPP; 11%), and regional vascular resistance in the left-ventricular, renal, and splan chnic circulations, while cardiac output decreased (CO; 23%) and skele tal muscle blood flow and vascular resistance were unaffected. Plasma norepinephrine and epinephrine increased by approximate to 30% and 90% , respectively. On separate days, the same hemodynamic responses were measured before and at 20 min of treadmill running during vehicle or n icotine infusion for the last 2 min of exercise (N = 10). Nicotine inc reased MAP (6%), SVR (14%), and RPP (3%), and elevated vascular resist ance in the proximal colon and pancreas. Moreover, compared to. exerci se + vehicle, norepinephrine and epinephrine increased by approximate to 13% and 24%, respectively, during exercise + nicotine infusion. The se findings suggest that the detrimental effects of nicotine observed at rest are minimized during exercise. Nicotine's effects may be reduc ed during exercise by competition from local vasodilators in the heart and active musculature, and/or by differing activation of sympathetic nerve activity.