Punzengruber C, Silberbauer K, Sinzinger H
Z Kardiol. 1986 Nov;75(11):676-81.
The mechanism of action by which nitrates produce vasodilation has not been fully clarified so far. Experimental studies indicate a possible relationship to the prostaglandin system. This study describes the consequences of acute prostaglandin synthesis inhibition on the hemodynamic effects of nitroglycerin in patients with stable angina pectoris. Intravenous application of 1 g acetylsalicylic acid was associated with a small but significant blunting of the pressure decline in the pulmonary and systemic circulation following the sublingual administration of 0.8 mg nitroglycerin. Premedication with 75 mg indomethacin i.m. was followed by a decrease in pressure decline in the pulmonary artery during intravenous nitroglycerin infusion. Significant inhibition of prostaglandin synthesis was shown by a substantial decline in plasma levels of circulating prostaglandin metabolites in both experiments. These results indicate that the mechanism of action of nitroglycerin may be partially mediated by vasodilatory prostaglandins.
迄今为止，硝酸盐产生血管舒张作用的机制尚未完全阐明。实验研究表明其可能与前列腺素系统有关。本研究描述了急性前列腺素合成抑制对稳定型心绞痛患者硝酸甘油血液动力学效应的影响。静脉注射1g阿司匹林与舌下含服0.8mg硝酸甘油后肺循环和体循环压力下降的轻微但显著减弱有关。肌肉注射75mg吲哚美辛进行预处理后，静脉输注硝酸甘油期间肺动脉压力下降减少。在两个实验中，循环前列腺素代谢物的血浆水平大幅下降表明前列腺素合成受到显著抑制。这些结果表明，硝酸甘油的作用机制可能部分由血管舒张性前列腺素介导。
