Clark K E, Farley D B, Van Orden D E, Brody M J
Am J Obstet Gynecol. 1977 Mar 1;127(5):455-61. doi: 10.1016/0002-9378(77)90434-3.
Earlier studies from these laboratories have demonstrated that prostaglandins (PG's) of the A and E series are potent uterine vasodilators whereas PGF's do not significantly alter uterine vascular resistance. In addition, PGE's and PGF's are also able to modify adrenergic vasoconstrictor responses in the canine uterus. In the present study the role of endogenous prostaglandins in regulating uterine vascular resistance and adrenergic neurotransmission was evaluated. Intra-arterial infusion of the prostaglandin synthesis inhibitor meclofenamate resulted in a significant reduction in PGE levels in uterine venous plasma and increased vascular resistance. Uterine vasoconstrictor responses produced by sympathetic nerve stimulation and norepinephrine were enhanced when endogenous PG synthesis was inhibited. During sympathetic nerve stimulation, uterine venous plasma levels of radioimmunoassayable prostaglandins of the E of F series did not change, suggesting that the adrenergic activation of PG synthesis is not detectable in uterine venous efferent. These data suggest that endogenous prostaglandins of the E series appear to play an important role in regulating uterine blood flow (I) by relaxing uterine vascular smooth muscle and (2) by depressing adrenergic vasoconstrictor responses.
这些实验室早期的研究表明，A 系列和 E 系列前列腺素（PG）是强效的子宫血管舒张剂，而前列腺素 F（PGF）不会显著改变子宫血管阻力。此外，前列腺素 E（PGE）和前列腺素 F（PGF）也能够改变犬子宫中的肾上腺素能血管收缩反应。在本研究中，评估了内源性前列腺素在调节子宫血管阻力和肾上腺素能神经传递中的作用。动脉内注入前列腺素合成抑制剂甲氯芬那酸导致子宫静脉血浆中 PGE 水平显著降低，并增加了血管阻力。当内源性 PG 合成受到抑制时，交感神经刺激和去甲肾上腺素产生的子宫血管收缩反应增强。在交感神经刺激期间，F 系列 E 型可通过放射免疫测定的前列腺素的子宫静脉血浆水平没有变化，这表明在子宫静脉流出物中无法检测到 PG 合成的肾上腺素能激活。这些数据表明，E 系列内源性前列腺素似乎在调节子宫血流中起重要作用：（1）通过舒张子宫血管平滑肌；（2）通过抑制肾上腺素能血管收缩反应。
