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前列腺素E在霍乱毒素诱导的肠道分泌中的作用。不存在中介作用。

Prostaglandin E in cholera toxin-induced intestinal secretion. Lack of an intermediary role.

作者信息

Hudson N, Hindi S E, Wilson D E, Poppe L

出版信息

Am J Dig Dis. 1975 Nov;20(11):1035-9. doi: 10.1007/BF01071191.

Abstract

Prostaglandin E1 (PGE1) and cholera enterotoxin stimulate small-intestine mucosal adenylate cyclase and intestinal secretion of water and electrolytes. The previous suggestion that PGE may mediate cholera-toxin effects was explored in these studies. Closed rabbit jejunal loops were injected in vivo with cholera toxin and compared to similar loops in the same animal injected with buffer. Loop mucosal homogenates and intestinal secretions were analyzed by radioimmunoassay for cAMP and PGE concentrations. Cholera toxin produced significant increases in mucosal and intestinal fluid cAMP; however, there were no significant increases in PGE in the toxin-treated loops when compared to the control loops. In addition, there was no correlation between cAMP and PGE in the same samples. These studies indicate that cholera toxin stimulates intestinal cAMP anc secretion independent of PGE synthesis and provide evidence against a specific role for PGE in mediating cholera-toxin effects.

摘要

前列腺素E1(PGE1)和霍乱肠毒素可刺激小肠黏膜腺苷酸环化酶以及水和电解质的肠道分泌。本研究探讨了先前提出的PGE可能介导霍乱毒素作用这一观点。给家兔体内的闭合空肠袢注射霍乱毒素,并与同一动物中注射缓冲液的类似肠袢进行比较。通过放射免疫分析法分析肠袢黏膜匀浆和肠分泌物中的cAMP和PGE浓度。霍乱毒素使黏膜和肠液中的cAMP显著增加;然而,与对照肠袢相比,毒素处理的肠袢中PGE没有显著增加。此外,同一样本中的cAMP和PGE之间没有相关性。这些研究表明,霍乱毒素刺激肠道cAMP和分泌独立于PGE合成,并提供了证据反驳PGE在介导霍乱毒素作用中具有特定作用的观点。

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