Fig. 8.

Ondansetron (Ondan) inhibits apamin-induced action potential duration at 80% repolarization (APD₈₀) prolongation in Anemonia sulcata II (ATX-II)-treated mouse hearts. A–D: intragroup comparisons of the effects of different experimental interventions on APD₈₀ at the pacing cycle lengths (PCLs) indicated. Data are means ± SE from 5 hearts in groups 1–3 and 3 hearts in group 4. In A, *P < 0.001 vs. baseline for all three PCLs; #P < 0.001 for PCL of 200 and 150 ms vs. PCL of 100 ms. In B, *P < 0.001 vs. baseline for all three PCLs; #P = 0.048 for PCL of 200 and 150 ms vs. PCL of 100 ms. In C, *P < 0.001 vs. baseline for all three PCLs; #P < 0.001 for PCL of 200 and 150 ms vs. PCL of 100 ms; †P < 0.001 vs. ondansetron vehicle + ATX-II for PCLs of 200 and 150 ms. E and F: intergroup comparisons of the effects of different experimental interventions on ∆APD₈₀ during the conditions indicated. Only values for PCLs of 150 and 200 ms are shown. E: magnitudes of ∆APD₈₀ induced by ATX-II alone were not significantly different between groups 1–3. F: ∆APD₈₀ sizes after exposure to ondansetron or apamin in the continuing presence of ATX-II (groups 1 and 2) were similar. Linear mixed models were used for statistical analyses with group, phase, and PCL as the fixed effects and mouse as the random effect. G: schematic presentation of the changes in APD in each experimental group.