Yanaka A, Ito S, Carter K J, Goddard P J, Silen W
Department of Surgery, Beth Israel Hospital, Boston, Massachusetts.
Am J Physiol. 1992 Mar;262(3 Pt 1):G405-19. doi: 10.1152/ajpgi.1992.262.3.G405.
The effects of gaseous hypoxia and reoxygenation on oxynticopeptic (OPC) and surface mucous cells (SMC) were examined in in vitro bullfrog gastric fundic mucosae mounted in Ussing chambers. Forskolin-stimulated H+ secretion, transmucosal potential difference (PD), and electrical resistance (R) were monitored in tissues incubated in HCO3(-)-free or HCO3(-)-containing buffer. At serosal pH (pHs) 7.2, 1 h of hypoxia with 100% N2 resulted in a decrease in PD, increase in R, and complete inhibition of H+ secretion. After 30 min of hypoxia, the morphology of OPC changed from the secretory to the nonsecretory state without recognizable cytopathology. Destructive changes in OPC increased progressively at pHs 7.2 as the hypoxic period was prolonged from 4 to 24 h. After 4 h of reoxygenation following 12-24 h of hypoxia, OPC remained necrotic and H+ secretion showed no recovery, whereas in some areas where SMC were exfoliated adjacent SMC showed epithelial restitution. The recovery of H+ secretion and PD during 2 h of reoxygenation after 4 h of hypoxia at pHs 6.0 and 6.8 was less than that at 7.2 and 8.0 and was greater in the presence of serosal HCO3- than its absence at pHs 7.2. These results suggest that, in in vitro frog gastric mucosa, 1) OPC are more vulnerable to hypoxia than SMC, 2) basolateral acidosis exaggerates hypoxic injury of OPC, and 3) serosal HCO3- protects OPC from hypoxic injury.
在安装于尤斯灌流小室中的体外牛蛙胃底黏膜中，研究了气态低氧和复氧对泌酸-胃蛋白酶（OPC）细胞和表面黏液细胞（SMC）的影响。在不含HCO₃⁻或含HCO₃⁻的缓冲液中孵育的组织中，监测了福斯高林刺激的H⁺分泌、跨黏膜电位差（PD）和电阻（R）。在浆膜pH（pHs）为7.2时，用100% N₂进行1小时低氧导致PD降低、R增加以及H⁺分泌完全抑制。低氧30分钟后，OPC的形态从分泌状态转变为非分泌状态，没有明显的细胞病理学变化。在pHs为7.2时，随着低氧时间从4小时延长至24小时，OPC的破坏性变化逐渐增加。在低氧12 - 24小时后复氧4小时，OPC仍坏死，H⁺分泌未恢复，而在一些SMC脱落的区域，相邻的SMC显示出上皮修复。在pHs为6.0和6.8时，低氧4小时后复氧2小时期间H⁺分泌和PD的恢复低于pHs为7.2和8.0时，并且在浆膜存在HCO₃⁻时比不存在时在pHs为7.2时的恢复更大。这些结果表明，在体外蛙胃黏膜中，1）OPC比SMC更容易受到低氧的影响，2）基底外侧酸中毒会加剧OPC的低氧损伤，3）浆膜HCO₃⁻可保护OPC免受低氧损伤。
