Abstract：
BACKGROUND:The intestinal epithelial tight junction restricts the paracellular permeation of ions and nonelectrolytes. We hypothesized that this function could be altered or disrupted during cellular adenosine triphosphate (ATP) depletion (chemical hypoxia). METHODS:T84 monolayers grown on permeable supports were studied by electrophysiologic and flux techniques. Mitochondrial and glycolytic inhibitors were used to deplete cellular ATP. RESULTS:Transepithelial resistance to passive ion flow (R) rapidly decreased to 36% of control values with chemical hypoxia, an effect that was reversible if control conditions were restored within 1 hour. As ATP levels declined, a transient Cl- secretory current developed but disappeared as ATP levels reached 5% of control values. Both the secretory current and fall in R were abolished when ambient Cl- was replaced with gluconate but not with Br- or NO3-, or when N-methylglucamine replaced Na+. Transepithelial flux of mannitol but not inulin was increased during ATP depletion. Dual Na(+)-mannitol flux analysis confirmed that the decrease in R was due to an increase in paracellular, not transcellular, permeability. Dilution potentials indicated altered charge selectivity of the junctional pathway. CONCLUSIONS:Chemical hypoxia in intestinal epithelial monolayers alters but does not disrupt the permselectivity properties of the junctional complex.
journal_name
Surgeryjournal_title
Surgeryauthors
Matthews JB,Smith JA,Tally KJ,Menconi MJ,Nguyen H,Fink MPsubject
Has Abstractpub_date
1994-08-01 00:00:00pages
150-7; discussion 157-8issue
2eissn
0039-6060issn
1532-7361journal_volume
116pub_type
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