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  • 1
    ISSN: 1432-2013
    Keywords: Antisecretory factor ; E. coli STa enterotoxin ; Acid microclimate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of challenge by Escherichia coli STa enterotoxin on pig jejunal mucosal surface pH was investigated in vivo. Exposure to STa resulted in a rapid and reversible alkalinisation (P 〈0.001) of the jejunal mucosa from 6.27±0.11 (5) to 6.89±0.03 (5). This action of STa is probably mediated through cyclic 3′5′-guanosine monophosphate (cGMP) since the 8-bromo analogue of cGMP induced the same effect as that observed after STa challenge. The action of STa on mucosal pH was partially inhibited by pre-administration of an antisecretory factor (ASF) preparation. The action of 8-bromo cGMP was unchanged by the presence of ASF. This implies that ASF inhibition occurs during the early stages of STa action prior to stimulation of guanylate cyclase. This effect of STa on the pig jejunal mucosal surface pH, or acid microclimate, may explain why weak acid supplementation of oral rehydration solutions can be ineffective in certain types of diarrhoeal disease.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of comparative physiology 163 (1994), S. 633-641 
    ISSN: 1432-136X
    Keywords: H+ secretion ; Avian colon ; Acid microclimate ; Carbonic anhydrase ; Gallus domesticus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Experiments were performed on isolated, stripped colonic epithelia of low-salt-adapted hens (Gallus domesticus) in order to characterize acid secretion by this tissue. With symmetric, weak buffer solutions, colonic epithelia acidified both mucosal and serosal sides. Titration measurements of the mucosal acidification rate (pH-stat technique) averaged 1.63±0.25 μEq·cm-2·h-1. Mucosal acidification was also evident in colons from high-salt-adapted birds and in low-salt-adapted coprodeum, but was completely abolished in the high-salt coprodeum. Mucosal acidification by low-salt-adapted colonic epithelium was unaffected by sodium replacement, mucosal amiloride (10-3 mol·l-1), and serosal ouabain (5x10-4 mol·l-1), although all three treatments significantly reduced or reversed the short-circuit current. Acetazolamide (10-3 mol·l-1, serosal) reduced mucosal acidification by 15% and simultaneously increased short-circuit current by a similar amount. Colonic epithelia incubated in glucose-free solutions had significantly lower acidification rates (0.59±0.13 μEq·cm-2·h-1, P〈0.002 versus controls) and addition of glucose (15 mmol·l-1), but not galactose, partially restored acidification to control levels. Anoxia (N2 gassing) completely inhibited short-circuit current, but reduced acidification by only 30%. A surface microclimate pH, nearly 2 pH units more acidic than the bath pH of 7.1–7.4 was measured in low-salt-adapted colon and coprodeum. The acid microclimate of both tissues was partially attenuated by adaptation to a high-salt diet. Colonic microclimate pH was dependent on the presence of glucose and sensitive to the bath pH. Histochemical staining for carbonic anhydrase localized this enzyme to cytoplasm and lateral margins of one subfraction of colonic cells, and to cytoplasm in a second subpopulation Intense staining was also evident in subepithelial capillaries. These results suggest that a large part of mucosal acidification and maintenance of the acid microclimate in hen colon may be dependent on glycolysis and metabolic acid production, although a smaller, electrogenic and acetazolamidesensitive component also appears to exist. This latter component may become more prominent under conditions of cellular acidification.
    Type of Medium: Electronic Resource
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