Lavanchy N, Martin J, Giacomelli M, Rossi A
Eur J Pharmacol. 1986 Jun 24;125(3):341-51. doi: 10.1016/0014-2999(86)90790-9.
We used 31P NMR spectroscopy to study the effect of acebutolol on the metabolic disturbances caused by ischaemia in the isolated rat heart. The intracellular acidosis and high-energy phosphate compound depletion induced by global low-flow ischaemia were significantly attenuated in the presence of acebutolol 2.7 X 10(-5) and 1.35 X 10(-4) M. The drug displayed no significant effect either at the 5.4 X 10(-6) M concentration or when administered as pretreatment to the animals (50 mg X kg-1, 120 and 60 min before isolating the heart). Since acebutolol had no effect on the contractility of the isolated rat heart at the 2.7 X 10(-5) M concentration the present results suggest that the mechanisms through which acebutolol exerts its effects on energy metabolism are not related to a reduction of cardiac work. The possible contribution of the membrane-stabilizing property of the drug is suggested by the fact that high concentrations are needed and that a short pretreatment had no effect.
我们使用31P核磁共振波谱法研究醋丁洛尔对离体大鼠心脏缺血所致代谢紊乱的影响。在存在2.7×10(-5)和1.35×10(-4)M醋丁洛尔的情况下,整体低流量缺血诱导的细胞内酸中毒和高能磷酸化合物耗竭显著减轻。该药物在5.4×10(-6)M浓度时或作为动物预处理给药时(在分离心脏前120和60分钟,50mg·kg-1)均未显示出显著效果。由于醋丁洛尔在2.7×10(-5)M浓度时对离体大鼠心脏的收缩性没有影响,目前的结果表明,醋丁洛尔对能量代谢发挥作用的机制与心脏做功的降低无关。需要高浓度以及短时间预处理无效这一事实提示了该药物膜稳定特性的可能作用。