The apical surface of canine chief cell monolayers resists H+ back-diffusion.
The apical surface of canine chief cell monolayers resists H+ back-diffusion.
复制标题
犬主细胞单层的顶端表面抵抗 H 反向扩散。
作者：
Sanders,MJ;Ayalon,A;Roll,M;Soll,AH
胃粘膜对酸和消化性损伤的抵抗力反映在对H+从胃腔到血液的反向扩散的抵抗力1，2。然而，这一“障碍”的性质仍未确定。使用Ussing室，我们现在已经研究了从分散的犬胃底主细胞制备的单层的酸屏障功能3。这些单层分泌胃蛋白酶原响应刺激4。我们发现，在顶端溶液topH 2酸化时，跨上皮电阻（R）增加2.6倍，单层细胞保持1：100，000 H+浓度梯度超过4小时。在酸化的顶侧溶液中加入阿司匹林会导致R迅速衰减，而基底侧溶液酸化至apH < 5.5也会导致R迅速衰减。哇巴因处理的单层细胞显示R的上升预期与顶端酸化，而电位差（V）和短路电流（Isc）基本上下降到零，表明不渗透H+。然而，如果哇巴因处理的单层的完整性被低apicalpH破坏，则H+渗透发生，由依赖于跨单层的H+梯度的Isc反映。提示主细胞顶面是H ~+扩散的一个非常严密的屏障，可能是抗酸消化损伤的重要因素。
The resistance of the gastric mucosa to acid and peptic injury is reflected by a resistance to the back-diffusion of H+from gastric lumen to blood1,2. The nature of this ‘barrier’, however, remains undefined. Using Ussing chambers, we have now studied the acid-barrier function of monolayers prepared from dispersed canine fundic chief cells3. These monolayers secrete pepsinogen in response to stimulation4. We found that, on acidification of the apical solution topH 2, transepithelial resistance (R) increased 2.6-fold and the monolayers maintained this 1:100,000 H+concentration gradient for more than 4 h. The addition of aspirin to the acidified apical solution caused a rapid decay inR, as did acidification of the basolateral solution to apH < 5.5. Ouabaintreated monolayers displayed the rise in R expected with apical acidification, while potential difference (V) and short-circuit current (Isc) decreased essentially to zero, indicating impermeability to H+. However, if the integrity of the ouabaintreated monolayers was disrupted by low apicalpH, H+permeation occurred, reflected by anIscthat was dependent on the H+gradient across monolayers. These data indicate that the apical surface of chief cells is a very tight barrier to H+diffusion and may be an important element resisting acid-peptic injury.