Miller R C, Cornish E J, Goldie R G
Pharmacol Res Commun. 1984 Jan;16(1):31-9. doi: 10.1016/s0031-6989(84)80102-2.
Indomethacin, 2.8 microM, potentiated relaxation responses of sheep, isolated, superfused coronary arteries caused by electrical transmural stimulation of sympathetic nerves by 2.3 fold, while responses to exogenous noradrenaline were not significantly altered. A ten fold higher concentration of indomethacin potentiated responses to sympathetic nerve stimulation by 3.4 fold and to exogenous noradrenaline by 1.8 fold. Stimulation-induced efflux of radioactivity derived from 3H-(-)-noradrenaline in sheep coronary arteries was not significantly altered by indomethacin (28 microM). Thus, while indomethacin-induced potentiation of relaxation responses to sympathetic nerve stimulation, was not due to an inhibition of prejunctional actions of prostaglandins, it may involve inhibition of the synthesis of prostaglandins which have post-junctional effects.
2.8微摩尔的消炎痛使绵羊离体灌流冠状动脉对交感神经经壁电刺激所产生的舒张反应增强了2.3倍，而对外源性去甲肾上腺素的反应则无明显改变。浓度高10倍的消炎痛使对交感神经刺激的反应增强3.4倍，对外源性去甲肾上腺素的反应增强1.8倍。消炎痛（28微摩尔）对绵羊冠状动脉中由3H-（-）-去甲肾上腺素引起的刺激诱导放射性流出无明显影响。因此，虽然消炎痛增强对交感神经刺激的舒张反应并非由于抑制前列腺素的节前作用，但可能涉及抑制具有节后效应的前列腺素的合成。
