Mentz P, Förster W
Arzneimittelforschung. 1984;34(12):1739-42.
In isolated perfused heart preparations of guinea pigs coronary dilating and positive inotropic doses of oxyfedrine induce a significant increase of the release of prostaglandin-like substances (PLS) and prostacyclin (PGI2). Indometacin as an inhibitor of prostaglandin biosynthesis (140 mumol/l) enhances after a 10 min lasting perfusion contraction force and coronary flow of the hearts but inhibits PGI2-formation. Under these conditions oxyfedrine loses its positive influence on inotropism, coronary flow and PGI2-efflux. Indometacin (140 mumol/l) also completely abolishes the increase of cardiac performance of isolated auricle preparations by oxyfedrine (50 mumol/l). These findings agree with former results and indicate an involvement of the PLS- and PGI2-biosynthesis in the antianginal efficacy of oxyfedrine.
在豚鼠离体灌流心脏标本中，冠状动脉扩张剂量和正性肌力剂量的奥昔非君可显著增加类前列腺素物质（PLS）和前列环素（PGI2）的释放。作为前列腺素生物合成抑制剂的吲哚美辛（140 μmol/L）在持续灌注10分钟后可增强心脏的收缩力和冠状动脉血流量，但会抑制PGI2的形成。在这些条件下，奥昔非君对心肌收缩力、冠状动脉血流量和PGI2流出的积极影响消失。吲哚美辛（140 μmol/L）也完全消除了奥昔非君（50 μmol/L）对离体心房标本心脏功能的增强作用。这些发现与之前的结果一致，表明PLS和PGI2生物合成参与了奥昔非君的抗心绞痛疗效。
