IVA changed atrial MAPD90, EPR and PRR in paced hearts
IVA, at high concentrations of 10 µM, prolonged the MAPD90, ERP and PRR when hears were paced a CL of 570 ms to maintain a stable heart rate before and after IVA infusion from 50.59 ± 2.55, 92.50 ± 5.23 and 44.29 ± 3.03 ms to 58.93 ± 1.21, 126.25 ± 7.14 and 68.57 ± 5.52 ms (n=13, p<0.05 vs. baseline; Fig 2A-a). When the hearts were paced at CL of 350 ms, IVA (0.3-10 μM) significantly prolonged atrial MAPD90 from 47.62 ± 1.72 to 62.08 ± 3.01 ms (n=13, p < 0.01 ; Fig. 2A), IVA at high concentrations of 3-10 μM prolonged the ventricular epi-cardial MAPD90 from 127.38 ± 4.37 ms to 151.27 ± 1.53 ms (n=6,p < 0.01 ), respectively.
ATX-II (2 nM) and ACh (0.3 μM) caused either prolongation or shortening of MAPD90, ERP and PRR, respectively, from 47.62 ± 1.72, 85.00 ± 3.45 and 40.75 ± 3.45 ms to 68.95 ± 4.03, 95.33 ± 2.76 and 22.83 ± 4.82, and 32.06 ± 1.83, 70.33 ± 1.09 and 38.33 ± 2.09 ms (n=18 and 21, respectively, p<0.05, Fig 2B-C). IVA (1-10 μM) prolonged the MAPD90 in control hearts (n=23,p<0.05 vs. baseline; Fig 1A-a) and ACh-treated hearts (n=21, p<0.05 vs. ACh alone; Fig 2C-a) but shortened the MAPD90 in ATX-II-treated hearts (n=18,p<0.05 vs. ATX-II alone; Fig 2B-a). For the ERP and PRR, IVA (1-10 μM) showed prolonging effects in all hearts (p<0.05 vs. baseline or ATX-II/ACh alone; Fig 2-b and 2-c). These results suggest that the effect of IVA on atrial electric parameters depends on hearts‘ substrate in rabbits.