Effects of Nicotine on Myocardial Metabolism and Performance in Dogs

Abstract

Nicotine infused i.v. is known to increase plasma free fatty acids (FFA). As increased delivery of FFA raises myocardial oxygen consumption (MVO₂) without influencing mechanical performance, the effect of nicotine i.v. on MVO₂ was studied before and during inhibition of lipolysis with β-pyridyl-carbinol. Although mechanical responses to nicotine –- evidenced by left ventricular pressure, maximal rate of rise of left ventricular pressure (dP/dt), cardiac output, and mean aortic blood pressure - rose similarly in both settings, MVO₂ increased by 4.1 ± 0.9 ml · min⁻¹ · 100 g⁻¹ (mean ± S.E.M.) before and 2.1 ± 0.6 ml · min⁻¹ · 100 g⁻¹ (P < 0.005) during inhibition of lipolysis. In conclusion about 50 per cent of the nicotine-induced rise in MVO₂ was related to enhanced mechanical activity of the heart, the remainder being attributable to a metabolic stimulation of high concentrations of FFA.

Key Words:

• β-pyridyl-carbinol
• free fatty acids
• glycerol
• lipolysis
• myocardial blood flow
• myocardial oxygen consumption