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缓激肽释放前列腺素作为其致痛作用的内在机制。

Release of prostaglandins by bradykinin as an intrinsic mechanism of its algesic effect.

作者信息

Lembeck F, Popper H, Juan H

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1976 Jul;294(1):69-73. doi: 10.1007/BF00692786.

Abstract
  1. The release of PGs from the isolated perfused rabbit ear was measured by means of a radioimmunoassay. 2. Bradykinin in dose dependent amounts released mainly PGE (presumably PGE1) and in much smaller amounts also PGF. 3. Bradykinin released similar amounts of PGE in innervated and chronically denervated ears. 4. Indomethacin completely prevented the PGE release by bradykinin. 5. ACh showed a much lower efficacy than bradykinin in releasing PGE and PGF. Synthetic substance P was devoid of any PGE releasing action. 6. It is concluded that bradykinin increases its own algesic action by a concomitant rapid stimulation of the PGE synthesis, thus providing a mechanism for the facilitation of its own algesic action.
摘要
  1. 通过放射免疫分析法测定了从离体灌注兔耳中释放的前列腺素。2. 剂量依赖性的缓激肽主要释放PGE(推测为PGE1),也释放少量的PGF。3. 缓激肽在有神经支配和长期去神经支配的耳朵中释放的PGE量相似。4. 吲哚美辛完全抑制了缓激肽引起的PGE释放。5. 乙酰胆碱在释放PGE和PGF方面的效力远低于缓激肽。合成的P物质没有任何释放PGE的作用。6. 得出的结论是,缓激肽通过同时快速刺激PGE合成来增强其自身的致痛作用,从而为促进其自身致痛作用提供了一种机制。

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