Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Oslo, Norway
Published September 1, 1971 - More info
The effect of intravenous infusion of isoproterenol on myocardial oxygen consumption (ṀVo2) was studied in 10 intact and anesthetized dogs before and after inhibition of lipolysis. In five dogs lipolysis was inhibited by nicotinic acid or beta pyridyl carbinol and in five other dogs by high plasma glucose concentrations. In spite of similar mechanical responses to isoproterenol, as evidenced by left ventricular pressure, maximal rate of rise of left ventricular pressure (dP/dt), heart rate and cardiac output, augmentation of ṀVo2 was larger before (on average 7.6 ml/min·100 g) than after inhibition of lipolysis either by antilipolytic drugs (on average 4.5 ml/min·100 g) (P < 0.005), or by high plasma glucose concentrations (on average 4.3 ml/min·100 g) (P < 0.02). As mechanical responses to isoproterenol were similar before and after inhibition of lipolysis, it is concluded that the additional rise in ṀVo2 with intact lipolysis was caused by a metabolic stimulation by high concentrations of free fatty acids.