1. Volume 118, Issue 6, Pages 1051-1060 (June 2000)
Identification of transport abnormalities in duodenal mucosa and duodenal enterocytes from patients with cystic fibrosis 
Vijaya S. Pratha, Daniel L. Hogan, Birgitta A. Martensson, Joie Bernard, Rihong Zhou, Jon I. Isenberg 
Gastroenterology 
Volume 118, Issue 6, Pages (June 2000)
DOI: /S (00)
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2. Fig. 1
Effect of db-cAMP on (A) HCO3− secretion and (B) Isc in duodenal mucosa from CF patients and NL subjects. Biopsy specimens were mounted in Ussing chambers, and increasing sequential concentrations of db-cAMP were added to the nutrient bath at 30-minute intervals. (A) A significant increase in the HCO3− secretory response to db-cAMP was observed in normal (NL; n = 8) tissues, whereas in CF (n = 6) tissues db-cAMP had no effect. (B) Similar results were observed with Isc responses. Results are mean ± SEM; *P < 0.05 vs. basal Wilcoxon signed-rank test. Results are means ± SEM for alternate data points for clarity; SEMs were consistent throughout.
Gastroenterology  , DOI: ( /S (00) )
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3. Fig. 2
Effect of carbachol on (A) HCO3− secretion and (B) Isc in duodenal biopsy specimens from CF patients and healthy subjects. Tissues were mounted in Ussing chambers, and increasing sequential concentrations of carbachol were added to the nutrient bath at 30-minute intervals. (A) In contrast to the findings with db-cAMP, carbachol resulted in a comparable increase in HCO3− secretion in both CF (5 of 6 patients; 1 no change) and NL (n = 8) tissues. (B) Although carbachol produced dose-related increases in Isc, no changes in Isc were observed in the CF tissues. Tissue resistance was unaltered after carbachol in the CF tissues (data not shown). Results are mean ± SEM; *P < 0.05 vs. basal, Wilcoxon signed-rank test. Results are means ± SEM for alternate data points for clarity; SEMs were consistent throughout.
Gastroenterology  , DOI: ( /S (00) )
Copyright © 2000 American Gastroenterological Association Terms and Conditions

4. Fig. 3
Effects of STa on (A) HCO3− secretion and (B) Isc in duodenal biopsy specimens from CF patients and healthy subjects. Increasing sequential concentrations of STa were added to the luminal bath at 30-minute intervals. (A) Increasing concentrations of STa resulted in similar increases in HCO3− secretion from basal in both CF (6 of 7 patients) and NL (n = 7) tissues. (B) In contrast to findings with carbachol (see Figure 2), STa produced a significant increase in Isc in 6 of 7 CF patients. Results are mean ± SEM; *P < 0.05 vs. basal, Wilcoxon signed-rank test. Results are means ± SEM for alternate data points for clarity; SEMs were consistent throughout.
Gastroenterology  , DOI: ( /S (00) )
Copyright © 2000 American Gastroenterological Association Terms and Conditions

5. Fig. 4
Net peak (A) HCO3− and (B) Isc responses from baseline to db-cAMP, carbachol (Carb), and STa. The bars represent the mean + SEM responses, and the circles indicate the individual net peak responses in CF (○) and NL (●) tissues. (A) db-cAMP (cAMP) had minimal effect on HCO3− secretion in CF compared with NL tissues, whereas both carbachol and STa produced similar significant increases in HCO3− secretion (P < 0.05, CF and NL, Wilcoxon signed-rank test). (B) Both cAMP and carbachol failed to stimulate Isc in CF compared with NL; however, STa produced similar significant increases in Isc in CF and NL duodenal tissues (P < 0.05, CF and NL, Wilcoxon signed-rank test). Note that 8 NL and 6 CF tissues were tested. Overlap of symbols occurred in some studies. *P < 0.05 vs. NL, Wilcoxon signed-rank test.
Gastroenterology  , DOI: ( /S (00) )
Copyright © 2000 American Gastroenterological Association Terms and Conditions

6. Fig. 5
Recovery of pHi from an acid load. Duodenocytes, isolated from CF and NL biopsy specimens, were superfused with either HEPES or RBB and prepulsed with 40 mmol/L NH4Cl for 2 minutes, and pHi recovery was quantitated. (A) In HEPES buffer, pHi recovery was comparable in both CF (n = 4 patients) and NL (n = 10 subsets; at least 8 randomly selected duodenal cells analyzed in each experiment) duodenal cells, indicating normal functioning Na+/H+ exchange in CF. (B) In RBB, pHi recovery was similar in CF (n = 6) and NL (n = 10) duodenocytes, indicating that both Na+/H+ exchange and NaHCO3 cotransport function normally in CF. The rate of pHi recovery, ΔpH/Δt, in RBB was significantly greater than recovery in HEPES buffer in both CF and NL duodenocyte. Results are mean ± SEM.
Gastroenterology  , DOI: ( /S (00) )
Copyright © 2000 American Gastroenterological Association Terms and Conditions

7. Fig. 6
Recovery of pHi from an induced alkaline load. Duodenocytes, isolated from CF and NL biopsy specimens, were superfused with RBB and prepulsed with 50 mmol/L sodium propionate (Prop) for 6 minutes, and pHi recovery was quantitated. (A) In RBB, pHi recovery was slightly more slow in CF (n = 8) than NL (n = 7) duodenocytes. (B) However, when Cl− (Cl−-free BB, gluconate substitution) was removed after a second sodium propionate pulse, pHi recovery was markedly impaired in CF compared with NL duodenocytes. Results are mean ± SEM. (Inset) Summary of pHi recovery rates, ΔpH/Δt, in CF (n = 8) and NL (n = 7) duodenocytes from induced alkaline loads. (A) The rate of pHi recovery in Cl−-containing RBB was similar in CF and NL duodenal cells. (B) In contrast, removal of Cl− significantly inhibited the rate of pHi recovery in CF cells, indicating a role for CFTR in alkaline extrusion. Results are mean ± SEM from calculated individual pHi recovery rates that were fitted to single exponential function using a nonlinear least-squares fitting procedure, as reported previously.
Gastroenterology  , DOI: ( /S (00) )
Copyright © 2000 American Gastroenterological Association Terms and Conditions