Schrör K, Krebs R, Nookhwun C
Eur J Pharmacol. 1976 Sep;39(1):161-9. doi: 10.1016/0014-2999(76)90124-2.
Experiments were performed in isolated guinea pig hearts, perfused at constant volume. Left ventricular pressure, left ventricular dp/dtmax, coronary vascular pressure and coronary venous pO2 were measured continuously. Indomethacin (1.4 X 10(-6) M) increased coronary vascular resistance by 15% over control (p less than 0.01) without altering the myocardial contractile force. When PGE2 (1.4 X10(-8) M) was subsequently added, it abolished the indomethacin action and lowered the coronary vascular resistance below the pre-indomethacin control value. This increase in coronary vascular resistance caused by indomethacin was also seen when the animals were pretreated with reserpine and/or the adrenoceptor blocking agents phenoxybenzamine and propranolol, but was prevented completely by previous addition of PGE2 (1.4 X 10(-7) M). The results provide evidence for possible involvement of endogenous prostaglandin-like substances in the maintenance of coronary vascular resistance in the isolated guinea pig heart.
实验在恒容灌注的离体豚鼠心脏上进行。连续测量左心室压力、左心室dp/dtmax、冠状血管压力和冠状静脉pO2。吲哚美辛(1.4×10⁻⁶M)使冠状血管阻力比对照组增加15%(p<0.01),而不改变心肌收缩力。随后加入前列腺素E2(1.4×10⁻⁸M)时,它消除了吲哚美辛的作用,并使冠状血管阻力降至吲哚美辛给药前的对照值以下。当动物用利血平、和/或肾上腺素能受体阻断剂酚苄明和普萘洛尔预处理时,也可见吲哚美辛引起的这种冠状血管阻力增加,但预先加入前列腺素E2(1.4×10⁻⁷M)可完全防止这种增加。这些结果为内源性前列腺素样物质可能参与维持离体豚鼠心脏冠状血管阻力提供了证据。