Feldman A M, Levine M A, Gerstenblith G, Kaufman K D, Baughman K L
J Cardiovasc Pharmacol. 1987 Apr;9(4):493-9. doi: 10.1097/00005344-198704000-00015.
Furosemide is an effective diuretic that initiates a rapid diuresis and peripheral vasodilatation through renal adenylate cyclase inhibition and prostaglandin synthesis. Recently, it has been shown to be associated with activation of the neurohumoral vasoconstrictor mechanism and a further compromise of left ventricular function in patients with heart failure. The present study was performed to investigate the direct effects of furosemide on myocardial performance in the isolated perfused rabbit heart. Furosemide (10(-3) M) caused a significant decrease in developed pressure as well as a similar fall in coronary perfusion pressure. Furosemide also decreased myocardial contractility when the coronary perfusion pressure was kept constant. The change in developed pressure but not the decrease in coronary perfusion pressure could be blocked by treatment with indomethacin. Furosemide did not antagonize rabbit cardiac membrane adenylate cyclase. Therefore, furosemide has a direct inhibitory effect on cardiac contractility that is related to prostaglandin synthesis.
速尿是一种有效的利尿剂，它通过抑制肾腺苷酸环化酶和合成前列腺素引发快速利尿和外周血管舒张。最近研究表明，在心力衰竭患者中，速尿与神经体液血管收缩机制的激活以及左心室功能的进一步受损有关。本研究旨在探讨速尿对离体灌注兔心脏心肌性能的直接影响。速尿（10⁻³ M）导致舒张期压力显著降低，同时冠状动脉灌注压也出现类似下降。当冠状动脉灌注压保持恒定时，速尿也会降低心肌收缩力。吲哚美辛处理可阻断舒张期压力的变化，但不能阻断冠状动脉灌注压的降低。速尿并不拮抗兔心脏膜腺苷酸环化酶。因此，速尿对心脏收缩力有直接抑制作用，且这种作用与前列腺素合成有关。
