TIMING OF UTERINE SENSITIVITY FOR THE DECIDUAL CELL REACTION - ROLE OF PROSTAGLANDINS
TIMING OF UTERINE SENSITIVITY FOR THE DECIDUAL CELL REACTION - ROLE OF PROSTAGLANDINS
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DOI：
10.1093/biolreprod/22.3.519
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发表时间：
1980-01-01
影响因子：
3.6
通讯作者：
KENNEDY, TG
中科院分区：
文献类型：
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作者：
KENNEDY, TG
子宫对蜕膜细胞反应敏感的时间可能与子宫产生前列腺素[PG]的能力有关，或者与子宫内膜血管通透性增加对PG做出反应的能力有关。对未成熟的大鼠进行激素治疗并切除卵巢，使其处于相当于假妊娠的第 4、5 或 6 天。这些治疗导致大鼠对蜕膜细胞反应有不同的敏感性。刺激子宫[单侧宫内注射50μl含有明胶的磷酸盐缓冲盐水(PBS-G)]后5天，对于第4、5和6天处理的大鼠，注射的子宫角平均重量分别为284、798和303mg。静脉注射后 15 分钟，受刺激角的放射性水平表明。注射[125I]标记的牛血清白蛋白（[125I]-BSA），子宫刺激后8小时子宫内膜血管通透性的增加在第5天处理的动物中也是最大的。与未注射子宫角的浓度相比，通过放射免疫测定法测定的PGE和PGF的子宫浓度在子宫内PBS-G处理后15分钟和2小时升高；然而，不同天数之间没有显着差异，这表明子宫内膜血管通透性反应的差异并不是由于子宫 PG 产生的差异造成的。为了测定子宫对PG的反应性，将10μg PGE 2 或其载体单侧注射到用吲哚美辛处理以抑制内源性PG产生的大鼠的子宫腔内。 8小时后使用[125I]-BSA量化子宫内膜血管通透性；在相当于假妊娠第 5 天时，给予 PGE2 的大鼠注射角中的放射性浓度最高。子宫对蜕膜细胞反应敏感的时间显然与子宫产生PG的能力无关，但可能与其对PG的反应能力有关。或者，时间可以通过通透性增加介质的产生来确定，除了PG之外，通透性增加介质对于子宫内膜血管通透性的变化可能是必需的。
The timing of uterine sensitivity for the decidual cell reaction may be related to the ability of the uterus to produce prostaglandins [PG], or to respond to PG with increased endometrial vascular permeability. Immature rats were treated with hormones and ovariectomized so that they were at the equivalent of either Day 4, 5 or 6 of pseudopregnancy. These treatments resulted in rats differentially sensitized for the decidual cell reaction; 5 days after stimulation of the uterus [unilateral intrauterine injection of 50 .mu.l phosphate buffered saline containing gelatin (PBS-G)], the injected uterine horns weighed on average 284, 798 and 303 mg for rats treated on days 4, 5 and 6, respectively. As indicated by radioactivity levels in the stimulated horn 15 min after the i.v. injection of [125I]-labeled bovine serum albumin ([125I]-BSA), the increase in endometrial vascular permeability 8 h after stimulation of the uterus was also greatest in animals treated on day 5. Compared with concentrations in the noninjected uterine horns, the uterine concentrations of PGE and PGF, determined by radioimmunoassays, were elevated 15 min and 2 h following intrauterine PBS-G treatment; however, there were no significant differences between days, suggesting that the differential endometrial vascular permeability responses were not due to differences in uterine PG production. To determine uterine responsiveness to PG, 10 .mu.g PGE2 or its vehicle were injected unilaterally into the uterine lumen of rats treated with indomethacin to inhibit endogenous PG production. [125I]-BSA was used 8 h later to quantify endometrial vascular permeability; the concentration of radioactivity was greatest in the injected horn of rats given PGE2 at the equivalent of day 5 of pseudopregnancy. The timing of the uterine sensitivity for the decidual cell reaction apparently is not related to the ability of the uterus to produce PG, but may be related to its ability to respond to PG. Alternatively the timing may be determined by the production of a permeability increasing mediator which, in addition to PG, may be essential for changes in endometrial vascular permeability.