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前列腺素不是肠道对霍乱毒素反应的介质。

Prostaglandins are not mediators of the intestinal response to cholera toxin.

作者信息

Smith G S, Warhurst G, Tonge A, Turnberg L A

出版信息

Gut. 1985 Jul;26(7):680-2. doi: 10.1136/gut.26.7.680.

Abstract

We have determined the release of prostaglandin E2 into the lumen of closed ileal loops in the rat and have measured the capacity of the mucosa to synthesise and degrade prostaglandin E2 both in control animals and after exposure to cholera toxin or bisacodyl. Exposure to cholera toxin caused no change in any of these measurements whereas bisacodyl caused an increase in the luminal PGE2 content. We conclude that the secretion stimulated by cholera toxin is not mediated by locally produced prostaglandins.

摘要

我们已测定前列腺素E2在大鼠闭合回肠肠袢肠腔内的释放,并测量了对照动物以及暴露于霍乱毒素或比沙可啶后黏膜合成和降解前列腺素E2的能力。暴露于霍乱毒素并未使这些测量值发生任何变化,而比沙可啶则使肠腔内前列腺素E2含量增加。我们得出结论,霍乱毒素刺激的分泌并非由局部产生的前列腺素介导。

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Distant intestinal stimulation by cholera toxin in rat in vivo.
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引用本文的文献

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3
Cholera and prostaglandins.霍乱与前列腺素。
Nature. 1971 Jun 25;231(5304):536. doi: 10.1038/231536a0.
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Effects of crude and pure cholera toxin on prostaglandin.
Prostaglandins. 1975 Jul;10(1):117-27. doi: 10.1016/0090-6980(75)90098-2.
10
PGE-mediated laxative effect of diphenolic laxatives.二酚类泻药的前列腺素E介导的缓泻作用。
Naunyn Schmiedebergs Arch Pharmacol. 1978 Dec;305(3):241-6. doi: 10.1007/BF00498817.

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