Prostaglandin I2 and Increased Endometrial Vascular Permeability Preceding the Decidual Cell Reaction
Prostaglandin I2 and Increased Endometrial Vascular Permeability Preceding the Decidual Cell Reaction
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蜕膜细胞反应前的前列腺素 I2 和子宫内膜血管通透性增加
DOI：
10.1007/978-94-011-7855-6_17
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发表时间：
1980
影响因子：
3.7
通讯作者：
C. Evans
中科院分区：
文献类型：
--
作者：
T. Kennedy;G. Barbe;C. Evans
在大鼠中研究了在蜕膜细胞反应之前子宫内膜血管通透性增加是由前列腺素I2而不是前列腺素E2介导的可能性。未成熟的大鼠用激素预处理，以便在子宫刺激时，它们对蜕膜细胞反应敏感。为了确定促蜕膜刺激是否导致子宫前列腺素I2增加，大鼠接受单侧子宫内注射50 μl含明胶的磷酸盐缓冲盐水，并在此后不同时间处死。用放射免疫测定法测定，注射后30 min、2 h和8 h，注射子宫角6-酮-前列腺素F1α的水平高于未注射子宫角，表明子宫产生前列腺素I2受到刺激。前列腺素E水平也在注射角升高。为了确定前列腺素I2在子宫内给药时是否能够增加子宫内膜血管通透性，用吲哚美辛处理以抑制内源性前列腺素合成的大鼠接受单侧子宫内注射溶剂（50 μl 0.01 M Tris，0.145 M NaCl，pH 9.0）、50 μg前列腺素I2或50 μg前列腺素E2。使用碱性pH试图减少前列腺素I2的分解。子宫内膜血管通透性指数（放射性浓度的比率，在注射到非注射子宫角静脉注射125碘标记的牛血清白蛋白后15分钟），测定4或8小时后。前列腺素I2在任何处死时间对指数均无显著影响，而前列腺素E2显著增加指数。前列腺素I2与前列腺素E2无显著相互作用。前列腺素12不能改变子宫内膜血管通透性，提示它不能介导由促蜕膜刺激引起的通透性增加。然而，由于前列腺素I2在中性pH下的不稳定性，不能消除前列腺素I2的这种可能作用。
The possibility that the increased endometrial vascular permeability which precedes the decidual cell reaction is mediated by prostaglandin I2 rather than prostaglandin E2 was investigated in rats. Immature rats were pretreated with hormones so that at the time of uterine stimulation they were sensitized for the decidual cell reaction. To determine if a deciduogenic stimulus resulted in increased uterine prostaglandin I2, rats received a unilateral intrauterine injection of 50 μl phosphate bufferedsaline containing gelatin, and were killed at varying times thereafter. As determined by radioimmunoassay, the levels of 6-keto-prostaglandin F1α were elevated in the injected uterine horns compared to the noninjectea horns 30 min, 2 h and 8 h after injection, suggesting that uterine production of prostaglandin I2 had beenstimulated. Prostaglandin E levels were also elevated in the injected horns. To determine if prostaglandin I2 was able to increase endometrial vascular permeability when given into the uterus, rats treated with indomethacin to inhibit endogenous prostaglandin synthesis received a unilateral intrauterine injection of either vehicle (50 μl 0.01M Tris, 0.145 M NaCl, pH 9.0), 50 μg prostaglandin I2 or 50 μg prostaglandin E2. The alkaline pH was used in an attempt to reduce the breakdown of prostaglandin I2. Endometrial vascular permeability indices (ratios of the concentrations of radioactivity in the injected to noninjected uterine horns 15 min after an intravenous injection of 125I-labelled bovine serum albumin) were determined 4 or 8 h later. Prostaglandin I2 had no significant effect on the indices at either time of sacrifice, whereas prostaglandin E2 significantly increased the indices. Prostaglandin I2,did not interact significantly with prostaglandin E2. The inability of prostaglandin 12 to alter endometrial vascular permeability suggests that it does not mediate the increase in permeability which results from a deciduogenic stimulus. However, because of the instability of prostaglandin I2 at neutral pH, this possible role for prostaglandin I2 cannot be eliminated.