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促胰液素对清醒大鼠胃酸分泌的抑制作用机制

The mechanism of inhibitory action of secretin on gastric acid secretion in conscious rats.

作者信息

Shimizu K, Li P, Lee K Y, Chang T M, Chey W Y

机构信息

Department of Medicine, University of Rochester Medical Center, NY, USA.

出版信息

J Physiol. 1995 Oct 15;488 ( Pt 2)(Pt 2):501-8. doi: 10.1113/jphysiol.1995.sp020984.

Abstract
  1. Secretin has been recognized as an important enterogastrone. In order to investigate the mechanism of secretin-induced inhibition of gastric acid secretion, the effects of both anti-somatostatin antibody and indomethacin on acid secretion were examined in conscious rats with gastric cannulas. 2. Secretin given intravenously at 5.6 pmol kg-1 h-1 inhibited profoundly the acid secretion stimulated by pentagastrin at 0.3 microgram kg-1 h-1. 3. When a rabbit antisomatostatin serum was given intravenously, it not only abolished the secretin-induced inhibition on the pentagastrin-stimulated acid secretion, but also augmented both basal and pentagastrin-stimulated acid secretion. 4. Indomethacin also significantly augmented basal acid secretion, starting 45 min after the drug delivery began. It reversed the secretin-induced inhibition but it did not augment the pentagastrin-stimulated acid secretion. 5. Neither antisomatostatin serum influenced prostaglandin E2-induced inhibition of the pentagastrin-stimulated acid secretion, nor did indomethacin affect the inhibition by somatostatin, suggesting strongly that the inhibition by somatostatin is not mediated by endogenous prostaglandins, nor is that by prostaglandins E2 mediated by endogenous somatostatin. 6. It is concluded that the inhibitory action of secretin on pentagastrin-stimulated gastric acid secretion is mediated by both somatostatin and prostaglandins in conscious rats. The two inhibitors do not seem to interact endogenously for the inhibition of acid secretion. While endogenous somatostatin exerts a tonic inhibitory effect on both basal and pentagastrin-simulated acid secretion, prostaglandins augment basal acid secretion only.
摘要
  1. 促胰液素已被公认为一种重要的肠抑胃素。为了研究促胰液素抑制胃酸分泌的机制,在有意识的胃插管大鼠中检测了抗生长抑素抗体和吲哚美辛对胃酸分泌的影响。2. 以5.6 pmol kg⁻¹ h⁻¹的剂量静脉注射促胰液素,可显著抑制以0.3 μg kg⁻¹ h⁻¹的剂量注射五肽胃泌素所刺激的胃酸分泌。3. 静脉注射兔抗生长抑素血清后,不仅消除了促胰液素对五肽胃泌素刺激的胃酸分泌的抑制作用,还增加了基础胃酸分泌和五肽胃泌素刺激的胃酸分泌。4. 吲哚美辛也显著增加基础胃酸分泌,在给药开始45分钟后开始起效。它逆转了促胰液素诱导的抑制作用,但没有增加五肽胃泌素刺激的胃酸分泌。5. 抗生长抑素血清既不影响前列腺素E2对五肽胃泌素刺激的胃酸分泌的抑制作用,吲哚美辛也不影响生长抑素的抑制作用,这强烈表明生长抑素的抑制作用不是由内源性前列腺素介导的,前列腺素E2的抑制作用也不是由内源性生长抑素介导的。6. 得出结论,在有意识的大鼠中,促胰液素对五肽胃泌素刺激的胃酸分泌的抑制作用是由生长抑素和前列腺素共同介导的。这两种抑制剂在抑制胃酸分泌方面似乎没有内源性相互作用。内源性生长抑素对基础胃酸分泌和五肽胃泌素刺激的胃酸分泌均有紧张性抑制作用,而前列腺素仅增加基础胃酸分泌。

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