Mjos O D
J Clin Invest. 1971 Sep;50(9):1869-73. doi: 10.1172/JCI106679.
The effect of intravenous infusion of isoproterenol on myocardial oxygen consumption (MVo(2)) 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 MVo(2) 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 MVo(2) with intact lipolysis was caused by a metabolic stimulation by high concentrations of free fatty acids.
在10只完整的麻醉犬中,研究了在抑制脂肪分解前后静脉输注异丙肾上腺素对心肌耗氧量(MVo₂)的影响。5只犬用烟酸或β-吡啶甲醇抑制脂肪分解,另外5只犬用高血浆葡萄糖浓度抑制脂肪分解。尽管对异丙肾上腺素的机械反应相似,如左心室压力、左心室压力最大上升速率(dP/dt)、心率和心输出量所证明的那样,但脂肪分解抑制前MVo₂的增加(平均7.6 ml/min·100 g)大于用抗脂解药物抑制脂肪分解后(平均4.5 ml/min·100 g)(P < 0.005),或高血浆葡萄糖浓度抑制脂肪分解后(平均4.3 ml/min·100 g)(P < 0.02)。由于脂肪分解抑制前后对异丙肾上腺素的机械反应相似,得出结论,完整脂肪分解时MVo₂的额外增加是由高浓度游离脂肪酸的代谢刺激引起的。