Taylor W M, Van de Pol E, Bygrave F L
Eur J Biochem. 1986 Mar 3;155(2):319-22. doi: 10.1111/j.1432-1033.1986.tb09493.x.
Interactions between phenylephrine-induced oxygen consumption, lactate and pyruvate output, and urea and glucose production were examined in perfused livers from fed or 48-h-fasted rats. Within 2 min of phenylephrine infusion, oxygen consumption in perfused livers was increased by approximately 40%. Increases in oxygen consumption induced by phenylephrine were essentially abolished in the presence of carboxyatractyloside, whereas those induced by dinitrophenol were still evident. Phenylephrine-induced increases in oxygen consumption were accompanied by enhanced rates of gluconeogenesis and ureogenesis in livers from fed or 48-h-fasted animals. These data indicate that phenylephrine-induced increases in respiration in perfused rat liver may result from an enhanced rate of mitochondrial oxidative phosphorylation in response to an increased cellular energy requirement.
在喂食或禁食48小时大鼠的灌注肝脏中,研究了去氧肾上腺素诱导的氧消耗、乳酸和丙酮酸输出以及尿素和葡萄糖生成之间的相互作用。在注入去氧肾上腺素的2分钟内,灌注肝脏中的氧消耗增加了约40%。在羧基苍术苷存在的情况下,去氧肾上腺素诱导的氧消耗增加基本消除,而二硝基苯酚诱导的氧消耗增加仍然明显。去氧肾上腺素诱导的氧消耗增加伴随着喂食或禁食48小时动物肝脏中糖异生和尿素生成速率的提高。这些数据表明,去氧肾上腺素诱导的灌注大鼠肝脏呼吸增加可能是由于细胞能量需求增加导致线粒体氧化磷酸化速率提高所致。