Terashita Z, Fukui H, Nishikawa K, Hirata M, Kikuchi S
Jpn J Pharmacol. 1982 Apr;32(2):351-8. doi: 10.1254/jjp.32.351.
The contribution of prostacyclin (PGI2) to the coronary vasodilating action of arachidonic acid (AA) and bradykinin (BK) was examined in isolated perfused guinea-pig hearts. The injection of Aa (100 to 1,000 ng) and BK (1 to 100 ng) into the heart resulted in a dose-dependent increase in the total amount of coronary flow and a release of 6-keto-prostaglandin F1alpha, a stable metabolite of PGI2. Both AA and BK showed weak positive chronotropic effects. In addition, higher doses (300 and 1,000 ng) of AA caused a transient reduction in the coronary flow rate, left ventricular systolic pressure, and left ventricular dp/dt. The changes in coronary flow, release of PGI2, and all cardiodynamic parameters induced by AA were abolished by pretreatment of the preparation with diclofenac-Na. On the other hand, the BK-induced increase in coronary flow rate was only partially reduced by diclofenac-Na when the release of 6-keto-prostaglandin F1alpha was completely inhibited. It is concluded that in isolated perfused guinea-pig hearts, BK has both PGI2-independent and PGI-2-dependent coronary vasodilating actions; the latter action is less than 25%, and the coronary vasodilating action of AA is mainly mediated via PGI2.
在离体灌注的豚鼠心脏中，研究了前列环素（PGI2）对花生四烯酸（AA）和缓激肽（BK）冠脉舒张作用的贡献。向心脏注射AA（100至1000 ng）和BK（1至100 ng）导致冠脉血流总量呈剂量依赖性增加，并释放出PGI2的稳定代谢产物6-酮-前列腺素F1α。AA和BK均显示出较弱的正性变时作用。此外，较高剂量（300和1000 ng）的AA导致冠脉流速、左心室收缩压和左心室dp/dt短暂降低。用双氯芬酸-Na预处理标本后，AA诱导的冠脉血流变化、PGI2释放以及所有心脏动力学参数的变化均被消除。另一方面，当6-酮-前列腺素F1α的释放被完全抑制时，双氯芬酸-Na仅部分降低了BK诱导的冠脉流速增加。结论是，在离体灌注的豚鼠心脏中，BK具有不依赖PGI2和依赖PGI-2的冠脉舒张作用；后者作用小于25%，且AA的冠脉舒张作用主要通过PGI2介导。
