Ventura U, Ceriani T, Moggio R
Scand J Gastroenterol Suppl. 1984;92:55-8.
Gastric mucosal barrier of 'in vivo' dogs with a Heidenhain pouch (HP) was broken by butyric acid (BA). Cimetidine intravenously (5 mg/kg/h) prevented HCl secretion. Unidirectional fluxes of H+ and Na+, passive mucosal permeability [evaluated with a low-molecular-weight substance, polyethylenglycole 200(PEG 200)] were increased by BA while transparietal potential difference (PD) was depressed. HCO3- secretion, measured as PCO2 in HP, was incremented . Intragastric perfusion of acetazolamyde (Az) increased loss of BA from HP and enhanced the rupture of gastric mucosa. HCO3- secretion was depressed by Az. Intragastric perfusion of gastric phosphodiesterases inhibitors, theophylline (Th) and 3-isobutyl-1-methylxanthine (IMX), recovered the resistance of gastric mucosa both to ions and PEG 200. Nevertheless HCO3- secretion remained high.
i) cytoprotection of gastric mucosa with either Th or IMX was effective to normalize its resistance to ions and low-molecular-weight substances; ii) increment of HCO3- secretion during cytoprotection was uncoupled with mechanisms dependent on membrane permeability.
用海登海因袋（HP）构建的“体内”犬胃黏膜屏障被丁酸（BA）破坏。静脉注射西咪替丁（5毫克/千克/小时）可抑制盐酸分泌。BA使H⁺和Na⁺的单向通量、被动黏膜通透性（用低分子量物质聚乙二醇200（PEG 200）评估）增加，同时跨壁电位差（PD）降低。以HP中的PCO₂衡量的HCO₃⁻分泌增加。胃内灌注乙酰唑胺（Az）增加了BA从HP的流失，并加剧了胃黏膜的破裂。Az使HCO₃⁻分泌减少。胃内灌注胃磷酸二酯酶抑制剂茶碱（Th）和3 - 异丁基 - 1 - 甲基黄嘌呤（IMX）可恢复胃黏膜对离子和PEG 200的抵抗力。然而，HCO₃⁻分泌仍然很高。
i）用Th或IMX对胃黏膜进行细胞保护可有效使其对离子和低分子量物质的抵抗力恢复正常；ii）细胞保护期间HCO₃⁻分泌的增加与依赖膜通透性的机制无关。
