Table 2.
BAs induce neither contraction nor relaxation in unstimulated (resting) airways
BA | Human | Mouse |
---|---|---|
DMSO | −2.6 ± 2.7 | −1.9 ± 0.2 |
CA | −5.3 ± 1.8 | −0.5 ± 0.3 |
GCA | ND | −1.3 ± 0.7 |
TCA | ND | 0.4 ± 0.4 |
CDCA | ND | −1.7 ± 1.0 |
GCDCA | ND | −0.4 ± 0.4 |
TCDCA | ND | 0.1 ± 0.5 |
LCA | ND | −0.2 ± 3.2 |
GLCA | ND | 6.4 ± 1.2 |
TLCA | −2.7 ± 3.7 | 1.0 ± 0.5 |
DCA | ND | −1.1 ± 0.5 |
GDCA | −5.2 ± 1.4 | −0.6 ± 0.4 |
TDCA | ND | −0.3 ± 0.4 |
UDCA | ND | −0.2 ± 0.4 |
Values are means ± SE of 3–5 precision-cut lung slices (PCLS) from 3 human lungs or 6–8 PCLS from 3 mice. Summary of decrease (+) or increase (−) in airway lumen area (%) induced by exposure of the PCLS to bile acids (BA; tested at 30 μM) or 0.1% DMSO (vehicle) in human and mouse peripheral airways at rest. The data were obtained from experiments similar to those shown in Fig. 1, A and D. There were no significant differences between groups; α = 0.05, one-way ANOVA. CA, cholic acid; CDCA, chenodeoxycholic acid; DCA, deoxycholic acid; GCA, glycocholic acid; GCDCA, glycochenodeoxycholic acid; GDCA, glycodeoxycholic acid; LCA, lithocholic acid; ND, not determined; TCA, taurocholic acid; TCDCA, taurochenodeoxycholic acid; TDCA, taurodeoxycholic acid; TLCA, taurolithocholic acid; UDCA, ursodeoxycholic acid.