Referenced in: none

Automatically associated channels: ClC4

Title: Gastric surface cell function: potential difference and mucosal barrier.

Authors: J M McGreevy

Journal, date & volume: Am. J. Physiol., 1984 Jul , 247, G79-87

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/6331194

Abstract
Rabbit fundic mucosa mounted in Ussing chambers for 4 h developed morphological deterioration of the gastric glands (GG), while the surface epithelial cell layer (SEC) remained intact. Since the tissues maintained a steady-state potential difference (PD) and resistance (R), it seemed that the surface cells might be responsible for both the PD and the R. To test this hypothesis, segments of fundic mucosa were exposed to selective anoxia by bubbling the mucosal (anoxic SEC) or serosal (anoxic GG) nutrient solutions with N2 instead of O2. Control tissues received O2 into both nutrient solutions. SEC anoxia resulted in a PD and short-circuit current (Isc) of zero within 10 min; R fell by 60% within 2 h. GG anoxia caused no change in PD or R over 2 h. Unidirectional fluxes (J) of 36Cl did not diminish as expected in tissues with no PD or Isc. This persistent JCl in tissues with a PD of zero was investigated in tissues with anoxic SEC. Simultaneous unidirectional fluxes of 36Cl and [3H]mannitol were determined to identify the transcellular (JClcell) and paracellular (JClleak) components of JCl during SEC anoxia. Similar flux measurements were made in control tissues (no anoxia). In control tissues, the calculated JClcell correlated with Isc (r = 0.72, n = 44). In tissues with anoxic SEC, the JClcell was 0.05 +/- 0.4 (mean +/- SD, n = 44). This series of experiments suggests that the PD and mucosal barrier characteristics of rabbit gastric mucosa in Ussing chambers are functions of a healthy surface cell layer.