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首页> 外文期刊>The Canadian journal of urology >Prostaglandin E mediates spontaneous rhythmic contraction in rabbit detrusor muscle.
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Prostaglandin E mediates spontaneous rhythmic contraction in rabbit detrusor muscle.

机译:前列腺素E介导兔逼尿肌自发性节律性收缩。

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INTRODUCTION: The purpose of this investigation was to determine if prostaglandin E(PGE) is produced by rabbit detrusor free of urothelium and demonstrate that PGE is responsible for the generation of spontaneous rhythmic contraction (SRC). METHODS: A bioassay was performed in which contraction frequency in strips of rabbit detrusor was compared before and after addition of superfusate from incubating sections of rabbit detrusor. Specificity was determined by testing the effects of SC-51089, a PGE(EP1) antagonist. Effects on development of tension were determined in artery segments after treatment with increasing doses of PGE, PGFalpha, and TXA, and a section of femoral artery was used as a negative control. Confirmation of PGE2 production was then determined using EIA kits. RESULTS: Increased rhythmic frequency was identified after superfusate from a section of rabbit detrusor free of urothelium was added to strips of detrusor from the same animal. Additional experiments demonstrated that rhythmic frequency generated after treatment with PGE was significantly reduced after treatment with SC-51089. In artery smooth muscle, prostaglandin dose response experiments demonstrated that only TXA induced contraction at physiologic doses (<10M). As a negative control, subsequent treatment of a section of femoral artery with detrusor superfusate failed to increase tension, confirming a lack of TXA production. EIA confirmed that PGE production increased by 4.8-fold in strips of detrusor free of urothelium after 15 minutes of incubation and that this production was blocked by ibuprofen and a COX-1 inhibitor. CONCLUSIONS: Rabbit detrusor produces PGE which is the most likely mediator of SRC.
机译:简介:本研究的目的是确定前列腺素E(PGE)是否由不含尿路上皮的兔逼尿肌产生,并证明PGE负责自发性节律性收缩(SRC)的产生。方法:进行生物测定,比较兔逼尿肌温育切片中添加超融合液前后兔逼尿肌条的收缩频率。通过测试PGE(EP1)拮抗剂SC-51089的作用来确定特异性。在增加剂量的PGE,PGFalpha和TXA处理后,确定了对动脉节段张力产生的影响,并将股动脉切片用作阴性对照。然后使用EIA试剂盒确定PGE2的产生。结果:将来自部分无尿路上皮的逼尿肌的超融合液添加到同一动物的逼尿肌条中后,发现节律频率增加。其他实验表明,用SC-51089治疗后,PGE治疗后产生的节律频率明显降低。在动脉平滑肌中,前列腺素的剂量反应实验表明,只有TXA可以在生理剂量(<10M)下引起收缩。作为阴性对照,随后用逼尿肌超融合液治疗股动脉段未能增加张力,从而证实缺乏TXA产生。 EIA确认,孵育15分钟后,在不含尿路上皮的逼尿肌条中,PGE的产量增加了4.8倍,并且该产量被布洛芬和COX-1抑制剂阻断。结论:兔逼尿肌产生PGE是最可能的SRC介体。

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