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  Indian J Med Microbiol
 

Figure 6: (A) Representative traces for inhibition of IhERG1bby fluoxetine 1 μM (Ai) chloroquine 1 μM (Aii) and cisapride 30 nM (Aiii) at 37°C. Lower panels show voltage protocols used. (B) Isochronal concentration-response relationships. Fluoxetine inhibited IhERG1bwith an IC50of 1.18 μM (confidence interval 0.87–1.60 μM) (nH = 1.23 [confidence interval 0.61–1.84]; n = 4–6 cells per concentration), chloroquine with an IC50of 1.11 μM (confidence interval 0.51–2.41 μM) (nH = 0.63 [confidence interval 0.28–0.94]; n = 4–5 cells per concentration) and cisapride with an IC50of 54.5 nM (confidence interval 37.6–79 nM) (nH = 1.2 [0.46–1.94]; n = 5–6 cells per concentration)

Figure 6: (A) Representative traces for inhibition of I<sub>hERG1b</sub>by fluoxetine 1 μM (Ai) chloroquine 1 μM (Aii) and cisapride 30 nM (Aiii) at 37°C. Lower panels show voltage protocols used. (B) Isochronal concentration-response relationships. Fluoxetine inhibited I<sub>hERG1b</sub>with an IC<sub>50</sub>of 1.18 μM (confidence interval 0.87–1.60 μM) (n<sub>H</sub> = 1.23 [confidence interval 0.61–1.84]; <i>n</i> = 4–6 cells per concentration), chloroquine with an IC<sub>50</sub>of 1.11 μM (confidence interval 0.51–2.41 μM) (n<sub>H</sub> = 0.63 [confidence interval 0.28–0.94]; <i>n</i> = 4–5 cells per concentration) and cisapride with an IC<sub>50</sub>of 54.5 nM (confidence interval 37.6–79 nM) (n<sub>H</sub> = 1.2 [0.46–1.94]; <i>n</i> = 5–6 cells per concentration)