[Studies on prostaglandin production relating to the mechanism of dysmenorrhea in endometriosis].

H Koike, T Ikenoue, N Mori
{"title":"[Studies on prostaglandin production relating to the mechanism of dysmenorrhea in endometriosis].","authors":"H Koike,&nbsp;T Ikenoue,&nbsp;N Mori","doi":"10.1507/endocrine1927.70.1_43","DOIUrl":null,"url":null,"abstract":"<p><p>The relationship between prostaglandins (PGs) production and the mechanism of dysmenorrhea in endometriosis is poorly understood. Consequently, we investigated the role of PGs in dysmenorrhea of endometriosis. Slices of normal endometrium, normal myometrium, adenomyosis, leiomyoma, normal ovary and affected ovary were incubated. 6-keto PGF1 alpha (a metabolite of PGI2), TXB2 (a metabolite of TXA2), PGF2 alpha and PGE2 concentrations of the incubation medium were measured by RIA. The results are as follows; 1) PGs production in endometriosis was significantly higher than that of other tissues, especially 6-keto PGF1 alpha, which was a dominant product in adenomyosis. 2) There were significant differences in PGs production between severe dysmenorrhea and non dysmenorrhea, especially tissue of adenomyosis with severe dysmenorrhea which produces large amounts of 6-keto PGF1 alpha. 3) There seems to be interaction between normal endometrium and normal myometrium with regard to 6-keto PGF1 alpha production. We concluded that increased PGI2 in the tissue of endometriosis seems to induce hyperalgesia during menstruation.</p>","PeriodicalId":19249,"journal":{"name":"Nihon Naibunpi Gakkai zasshi","volume":"70 1","pages":"43-56"},"PeriodicalIF":0.0000,"publicationDate":"1994-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1507/endocrine1927.70.1_43","citationCount":"13","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nihon Naibunpi Gakkai zasshi","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1507/endocrine1927.70.1_43","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 13

Abstract

The relationship between prostaglandins (PGs) production and the mechanism of dysmenorrhea in endometriosis is poorly understood. Consequently, we investigated the role of PGs in dysmenorrhea of endometriosis. Slices of normal endometrium, normal myometrium, adenomyosis, leiomyoma, normal ovary and affected ovary were incubated. 6-keto PGF1 alpha (a metabolite of PGI2), TXB2 (a metabolite of TXA2), PGF2 alpha and PGE2 concentrations of the incubation medium were measured by RIA. The results are as follows; 1) PGs production in endometriosis was significantly higher than that of other tissues, especially 6-keto PGF1 alpha, which was a dominant product in adenomyosis. 2) There were significant differences in PGs production between severe dysmenorrhea and non dysmenorrhea, especially tissue of adenomyosis with severe dysmenorrhea which produces large amounts of 6-keto PGF1 alpha. 3) There seems to be interaction between normal endometrium and normal myometrium with regard to 6-keto PGF1 alpha production. We concluded that increased PGI2 in the tissue of endometriosis seems to induce hyperalgesia during menstruation.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
[前列腺素分泌与子宫内膜异位症痛经机制的研究]。
前列腺素(pg)的产生与子宫内膜异位症痛经的机制之间的关系尚不清楚。因此,我们研究了PGs在子宫内膜异位症痛经中的作用。培养正常子宫内膜、正常子宫肌层、子宫腺肌病、平滑肌瘤、正常卵巢及病变卵巢切片。采用RIA法测定培养液中6-酮PGF1 α (PGI2的代谢物)、TXB2 (TXA2的代谢物)、PGF2 α和PGE2的浓度。研究结果如下:1)子宫内膜异位症的PGs产生量明显高于其他组织,尤其是6-酮PGF1 α,是子宫腺肌症的优势产物。2)重度痛经与非痛经组织中PGs的产生有显著差异,尤其是重度痛经的子宫腺肌病组织中PGs的大量产生6-酮PGF1 α。3)在6-酮PGF1 α的产生方面,正常子宫内膜和正常子宫肌层之间似乎存在相互作用。我们的结论是,子宫内膜异位症组织中PGI2的增加似乎会引起月经期间的痛觉过敏。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
[Parathyroid hormone]. [Treatment of hypothalamic-pituitary tumors--experiences at Hiroshima University School of Medicine]. [Future aspects on endocrinology]. [A view of basic endocrinology]. [Comment by a surgeon on Japan Endocrine Society, its past and future].
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1