Okuda M, Muneyuki M, Sogabe T, Miura I
Department of Anesthesiology, Mie University, School of Medicine, Tsu, Japan.
J Anesth. 1989 Sep 1;3(2):200-9. doi: 10.1007/s0054090030200.
The effects of dopamine, epinephrine and norepinephrine on energy metabolism as well as intracellular pH in rat liver and brain during hemorrhagic shock were examined by in vivo 31P-NMR spectroscopy. The hemorrhagic shock was induced by arterial bleeding to a mean arterial pressure (MAP) of 30-40 mmHg. Upon the induction of hemorrhagic shock, there was a dramatic fall in adenosine triphosphate (ATP) and a rise in inorganic phosphate (Pi) in the liver. The intracellular pH indicated severe acidosis. However, no change in these parameters was observed in the brain during hemorrhagic shock. After infusion of the above catechollamines following 10 min of hemorrhagic shock, MAP increased to 90-100% of its control value. Only dopamine improved hepatic energy metabolism, whereas brain energy metabolism was not affected by any of them. This suggests that dopamine protects liver function during hemorrhagic shock without affecting brain energy metabolism.
通过体内31P-核磁共振波谱法,研究了多巴胺、肾上腺素和去甲肾上腺素对失血性休克大鼠肝脏和大脑能量代谢以及细胞内pH值的影响。通过动脉放血使平均动脉压(MAP)降至30 - 40 mmHg来诱导失血性休克。诱导失血性休克后,肝脏中的三磷酸腺苷(ATP)急剧下降,无机磷酸盐(Pi)升高。细胞内pH值显示出严重酸中毒。然而,在失血性休克期间大脑中的这些参数未观察到变化。在失血性休克10分钟后输注上述儿茶酚胺后,MAP升至其对照值的90 - 100%。只有多巴胺改善了肝脏能量代谢,而大脑能量代谢不受它们中任何一种的影响。这表明多巴胺在失血性休克期间保护肝功能而不影响大脑能量代谢。