Li P, Chang T M, Chey W Y
Konar Center for Digestive and Liver Diseases, University of Rochester Medical Center, Rochester, New York 14626, USA.
Am J Physiol. 1998 Jul;275(1):G22-8. doi: 10.1152/ajpgi.1998.275.1.G22.
Secretin is an enterogastrone that inhibits gastric acid secretion and motility. Recently, it was reported that secretin inhibited gastric emptying via a capsaicin (Cap)-sensitive vagal afferent pathway. However, a possible role of the sensory afferent pathway in secretin-inhibited acid secretion has not been clarified. We investigated whether or not the acid secretion suppressed by secretin is modulated by a vagal and/or splanchnic afferent pathway in rats. Subdiaphragmatic perivagal (PV) or periceliac ganglionic (PCG) application of Cap (10 mg/ml) or vehicle was performed in both conscious and anesthetized rats 2 wk before experiments. Bilateral vagotomy was performed in some conscious rats 5 days before studies. Pentagastrin was administered intravenously at 0.6 microg . kg-1 . h-1. Secretin (20 pmol . kg-1 . h-1 iv) or 0.03 N HCl (4.32 ml/h id) was infused in conscious rats with gastric cannulas or anesthetized rats with ligation of the pylorus, respectively. A rabbit antisecretin serum was injected in some anesthetized rats before duodenal acidification. Secretin significantly inhibited pentagastrin-stimulated acid secretion by 63% (P < 0.01), which was abolished by both vagotomy and PV treatment of Cap in conscious rats. In anesthetized rats, duodenal infusion of 0.03 N HCl suppressed pentagastrin-induced acid secretion by 59.4% (P < 0.01), which was reversed not only by antisecretin serum but also by PV application of Cap. However, PCG treatment with Cap did not influence the inhibition by secretin or duodenal acidification in either awake or anesthetized rats. These results indicate that the inhibition by secretin of pentagastrin-stimulated acid secretion is mediated by a Cap-sensitive vagal afferent pathway but not via a splanchnic afferent pathway in rats.
促胰液素是一种肠抑胃素，可抑制胃酸分泌和胃蠕动。最近，有报道称促胰液素通过辣椒素（Cap）敏感的迷走神经传入途径抑制胃排空。然而，感觉传入途径在促胰液素抑制胃酸分泌中可能发挥的作用尚未阐明。我们研究了促胰液素抑制的胃酸分泌是否受大鼠迷走神经和/或内脏神经传入途径的调节。在实验前2周，对清醒和麻醉大鼠进行膈下迷走神经周围（PV）或腹腔神经节周围（PCG）注射Cap（10 mg/ml）或赋形剂。在一些清醒大鼠研究前5天进行双侧迷走神经切断术。以0.6 μg·kg-1·h-1的剂量静脉注射五肽胃泌素。分别对有胃插管的清醒大鼠或幽门结扎的麻醉大鼠输注促胰液素（20 pmol·kg-1·h-1静脉注射）或0.03 N HCl（4.32 ml/h十二指肠内注射）。在一些麻醉大鼠十二指肠酸化前注射兔抗促胰液素血清。促胰液素显著抑制五肽胃泌素刺激的胃酸分泌达63%（P<0.01），清醒大鼠的迷走神经切断术和PV注射Cap均可消除这种抑制作用。在麻醉大鼠中，十二指肠输注0.03 N HCl可使五肽胃泌素诱导的胃酸分泌抑制59.4%（P<0.01），不仅抗促胰液素血清可逆转这种抑制，PV注射Cap也可逆转。然而，PCG注射Cap对清醒或麻醉大鼠中促胰液素的抑制作用或十二指肠酸化均无影响。这些结果表明，在大鼠中，促胰液素对五肽胃泌素刺激的胃酸分泌抑制作用是由Cap敏感的迷走神经传入途径介导的，而非通过内脏神经传入途径。
