Manku M S, Mtabaji J P, Horrobin D F
Prostaglandins. 1977 Apr;13(4):701-9. doi: 10.1016/0090-6980(77)90242-8.
Concentrations of PGE1, PGE2, PGA1, PGA2 and PGF2alpha ranging from 10 to 10(5) pg/ml (2.8 x 10(-11) to 2.8 x 10(-7)M) were perfused through a rat mesenteric vascular bed preparation and their effects on baseline pressure and responses to noradrenaline noted. PGs A2 and FEalpha elevated baseline pressure at concentrations of 100 pg/ml and above but the other three PGs had little or no effect. PGs E2, A1 and F2alpha markedly potentiated responses to noradrenaline at all concentrations studied. In contrast PGs E1 and A2 caused a clear potentiation at 10 pg/ml but at higher concentrations the effect disappeared and concentrations of above 10(4) pg/ml were actually inhibitiory. E1 could antagonize the vascular effects of E2. These results offer possible explanations for some of the confusing findings reported in the literature.
将浓度范围为10至10⁵ pg/ml(2.8×10⁻¹¹至2.8×10⁻⁷M)的前列腺素E1、前列腺素E2、前列腺素A1、前列腺素A2和前列腺素F2α灌注通过大鼠肠系膜血管床标本,并记录它们对基础压力以及对去甲肾上腺素反应的影响。前列腺素A2和F2α在浓度为100 pg/ml及以上时会升高基础压力,但其他三种前列腺素几乎没有影响或没有影响。在所有研究浓度下,前列腺素E2、A1和F2α均显著增强对去甲肾上腺素的反应。相比之下,前列腺素E1和A2在10 pg/ml时引起明显增强,但在更高浓度时这种作用消失,且浓度高于10⁴ pg/ml时实际上具有抑制作用。E1可拮抗E2的血管效应。这些结果为文献中报道的一些令人困惑的发现提供了可能的解释。