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花生四烯酸、前列腺素E1和前列腺素E2在大鼠体内引起小肠液分泌的潜在机制。

Mechanisms underlying the small intestinal fluid secretion caused by arachidonic acid, prostaglandin E1 and prostaglandin E2 in the rat in vivo.

作者信息

Brunsson I, Sjöqvist A, Jodal M, Lundgren O

出版信息

Acta Physiol Scand. 1987 Aug;130(4):633-42. doi: 10.1111/j.1748-1716.1987.tb08186.x.

Abstract

Prostanoids were given intraluminally (PGE2) or infused close intra-arterially (PGE1 and PGE2) or arachidonic acid was administered intraluminally to denervated jejunal segments of the rat in vivo. These experimental manoeuvres caused a net fluid secretion, although a 1,000-fold higher concentration of the prostanoids was needed from the luminal than from the vascular side. I.v. hexamethonium or serosally applied lidocaine diminished the induced fluid secretion suggesting that the prostanoids act mainly by eliciting local secretory reflexes in the enteric nervous system. This nerve-mediated secretion is not accompanied by any increase in tissue cAMP. However, at higher i.a. concentrations of PGE2 there seems to be a non-neurogenic effect on the enterocytes associated with an increase in tissue cAMP.

摘要

在体内对大鼠去神经支配的空肠段管腔内给予前列腺素(PGE2),或经动脉内近距离输注(PGE1和PGE2),或管腔内给予花生四烯酸。这些实验操作引起了净液体分泌,尽管管腔内所需前列腺素的浓度比血管侧高1000倍。静脉注射六甲铵或浆膜面应用利多卡因可减少诱导的液体分泌,提示前列腺素主要通过引发肠神经系统中的局部分泌反射起作用。这种神经介导的分泌并不伴有组织cAMP的任何增加。然而,在较高的动脉内PGE2浓度下,似乎对肠上皮细胞有非神经源性作用,伴有组织cAMP增加。

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