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Figure 6 Effects of acetylcholine (ACh) on conduction velocity (CV) and transmembrane potential (TMP) characteristics. (A and B) Data from tissue no. 8 show that ACh had no effect on the CV during S₁ pacing. The CV along a central line during baseline and ACh (5 µmol/l) infusion was 94 cm/s. (C to F) A series of TMP recordings during different concentrations of ACh (data from tissue no. 10). (C) At baseline (no ACh), the action potential duration (APD₉₀) during S₁ pacing was 123 ms. There were only short runs of repetitive beats (<5 beats) induced. (D) During the infusion of 1 µmol/l of ACh, the APD₉₀ was shortened to 70 ms. The S₂ pacing induced a stable re-entry, anchoring to a large pectinate muscle (see Figs. 1B and 2). (E) Once ACh was raised to 2.5 µmol/l, the APD₉₀ was shortened to 50 ms. The S₂ pacing consistently induced nonstationary re-entry with a moving core (see Fig. 3). Note that during fibrillation, TMP recordings with variable APD₉₀ values and low amplitudes were frequently observed (vertical arrows). (F) However, by further shortening the APD₉₀ to 22 ms during 5 µmol/l of ACh infusion, multiple, but stationary wave fronts were induced by S₂ pacing (see Fig. 5). The APD₉₀ values and amplitudes of TMP recordings became relatively constant. PCL = pacing cycle length.