Marques M C, Ladosky E M, Fonteles M C
Braz J Med Biol Res. 1983 Jul;16(2):133-40.
The presynaptic effects of aspirin and prostaglandin E2 (PGE2) were evaluated in the isolated perfused cat heart preparation. Tissue catecholamine stores were studied by labelling the sympathetic nerve endings with [3H]-noradrenaline ([3H]-NA) and the effect of electric neural stimulation (5 Hz, 0.5 ms, 8 V, 60 s) was determined in the presence of drugs which inhibit neuronal or extraneuronal uptake, or antagonize alpha-adrenoceptors. [3H]-NA overflow was significantly increased by electric neural stimulation. Perfusion with 0.1 microM phentolamine increased transmitter overflow. Infusion of 0.1 microM PGE2 reduced the [3H]-NA overflow induced by electrical stimulation. Administration of 1 microM aspirin increased the [3H]-NA overflow and PGE2 prevented this effect of aspirin. The results support the view that PGEs participate in the negative feedback of transmitter release in the isolated perfused cat heart.
在离体灌注猫心脏标本中评估了阿司匹林和前列腺素E2(PGE2)的突触前效应。通过用[3H]-去甲肾上腺素([3H]-NA)标记交感神经末梢来研究组织儿茶酚胺储备,并在存在抑制神经元或神经元外摄取或拮抗α-肾上腺素能受体的药物的情况下,测定电神经刺激(5Hz,0.5ms,8V,60s)的效果。电神经刺激使[3H]-NA溢出显著增加。用0.1μM酚妥拉明灌注可增加递质溢出。输注0.1μM PGE2可减少电刺激诱导的[3H]-NA溢出。给予1μM阿司匹林可增加[3H]-NA溢出,而PGE2可预防阿司匹林的这种作用。结果支持了PGE参与离体灌注猫心脏中递质释放负反馈的观点。