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. 2002 Jun 1;541(Pt 2):411–421. doi: 10.1113/jphysiol.2002.019562

Table 2.

Effects of cytochalasin D and phalloidin on APD

APD25 (ms) APD50 (ms) APD75 (ms) APD90 (ms)
Normal (n = 3)
  Control 8.2 ± 0.7 15.2 ± 2.4 26.7 ± 4.1 44.2 ± 4.4
  Cyto D (50 μM) 8.9 ± 0.9 15.3 ± 3.2 31.7 ± 4.1 46.5 ± 5.8
  Cyto D + phalloidin (20 μM) 8.1 ± 0.6 15.8 ± 2.2 30.2 ± 3.7 45.4 ± 1.1
LVH (n = 5)
  Control 18.1 ± 2.8 39.6 ± 4.8 76.4 ± 18.4 105.7 ± 18.8
  Cyto D (50 μM) 30.9 ± 1.9* 74.6 ± 17.9* 136.7 ± 22.3* 181.1 ± 15.5*
  Cyto D + phalloidin (20 μM) 24.0 ± 1.6** 46.5 ± 5.9** 88.3 ± 12.3** 130.1 ± 6.8**
*

P < 0.05 compared to LVH control

**

P < 0.05 compared to LVH Cyto D. The results of a series of experiments using 50 μM cytochalasin D followed by 20 μM phalloidin are summarized. Note the prolonged APD of LVH cells. Exposure to 50 μM cytochalasin D has no effect on APD25–90 of normal cells (10 min). Subsequent exposure to phalloidin (20 μM) (maintaining cytochalasin D superfusion) has no effect on APD25–90 of the normal cell. In contrast, 50 μMcytochalasin D produces significant lengthening of APD25–90 in LVH cells at 10 min exposure. While maintaining 50 μM cytochalasin D, exposure to 20 μM phalloidin (10 min) significantly but only partially reverses the APD25–90 prolongation noted during exposure to cytochalasin D. Similar results were obtained in four other paired experiments.