Cardiac Effects of Nicotine in Dogs

Abstract

To examine how nicotine increases left ventricular stroke volume despite a concomitant rise in aortic blood pressure, the effects of nicotine and aortic constriction were compared in 11 anesthetized open-chest dogs whose myocardial dimensions were measured by ultrasound elements sewn into the ventricular wall. Stroke volume was increased by 22 ± 7% (mean ± S.E.M.; P < 0.02) during infusion of nicotine (20–25 μg · kg⁻¹ · min⁻¹). Simultaneously, left ventricular end-diastolic pressure (LVEDP) and end-diastolic myocardial chord length (EDMCL) increased (P < 0.005), as did systolic myocardial shortening (MS) (P < 0.01) and myocardial contractility (P < 0.001). Left ventricular systolic pressure (LVSP) rose by 37 ± 5 mm Hg (P < 0.001) during the infusion of nicotine. When a similar increase in LVSP was effected by aortic constriction, stroke volume was reduced by 12 ± 4% (P < 0.01), and LVEDP and EDMCL increased significantly more than during the nicotine infusion, whereas MS and myocardial contractility remained unchanged or slightly reduced. Thus, nicotine simultaneously affects cardiac contraction by two different mechanisms: increased contractility and increased afterload. A more complete systolic emptying of the left ventricle as a consequence of increased inotropy during nicotine infusion could mechanically explain the increased stroke volume despite an accompanying raised resistance to ventricular ejection.

Key Words:

• Afterload
• aortic constriction
• cardiac dimensions
• left ventricular pressure
• myocardial contractility
• nicotine
• stroke volume