Farley D B, Van Orden D E
Prostaglandins. 1982 May;23(5):657-74. doi: 10.1016/s0090-6980(82)80005-1.
A role for prostacyclin (PGI2) as a mediator of estrogen-induced increases in uterine blood volume (UBV) was investigated by measuring uterine tissue levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF 1 alpha), and testing estrogen responses in rats pretreated with the PGI2 synthesis inhibitor, tranylcypromine (TCP). Uterine 6-keto-PGF1 alpha content was determined by radioimmunoassay of tissue extracts purified through the use of high-performance liquid chromatography (HPLC). Estrogen treatment of castrate rats resulted in a significant increase of uterine 6-keto-PGF 1 alpha was compared to saline treated controls (9.3 ng/uterine horn vs 6.7 ng/uterine horn, p=0.01). Pretreatment with TCP (20 mg/kg) markedly reduced the uterine content of 6-keto-PGF 1 alpha (2.5 ng/uterine horn). The typical 50% increase in UBV observed after estrogen was unaffected by tranylcypromine pretreatment. It was concluded that the increased PGI2 synthesis, as indicated by elevated levels of 6-keto-PGF1 alpha, may function as an amplifying mechanism for the uterine vasodilation-induced by estrogen in castrate rats, but that production of this prostanoid is not essential for the estrogen response.
通过测量子宫组织中6-酮-前列腺素F1α（6-keto-PGF1α）的水平，并在给予前列环素（PGI2）合成抑制剂反苯环丙胺（TCP）预处理的大鼠中测试雌激素反应，研究了PGI2作为雌激素诱导子宫血容量（UBV）增加的介质的作用。通过使用高效液相色谱（HPLC）纯化组织提取物的放射免疫测定法测定子宫6-酮-PGF1α含量。与盐水处理的对照组相比，雌激素处理去势大鼠导致子宫6-酮-PGF1α显著增加（9.3 ng/子宫角对6.7 ng/子宫角，p = 0.01）。用TCP（20 mg/kg）预处理显著降低了子宫6-酮-PGF1α的含量（2.5 ng/子宫角）。雌激素后观察到的UBV典型的50%增加不受反苯环丙胺预处理的影响。得出的结论是，如6-酮-PGF1α水平升高所示，PGI2合成增加可能作为去势大鼠中雌激素诱导的子宫血管舒张的放大机制，但这种前列腺素的产生对于雌激素反应不是必需的。
