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When the frequency was fixed at 1 Hz, lidocaine, nifedipine, diltiazem, nicorandil ([I.sub.KATP] activator), Ni[Cl.sub.2], and the hypotonic ([I.sub.Cl-vol] activator) and high [[[Na.sup.+]].sub.i] solution shortened APD50 and APD90. The [I.sub.to] blocker 4-AP, [I.sub.Kr] blockers E-4031 and sotalol, and [I.sub.Ks] blocker chromalol 293B prolonged APD50 and APD90.
Acidosis reduced frequency and [V.sub.max] (the maximal depolarization velocity) and shortened APD50 and APD90 (repolarization of AP at 50 and 90%) but did not influence the RP (resting potential) and APA (amplitude of AP) (Figures 1(c)-1(h)).
Lidocaine and Ni[Cl.sub.2] shortened APD50 more strongly than they did on APD90, suggesting minor effects of [I.sub.Na] and [I.sub.NCX] on the late phase of APD.
Representative traces of APs (c), mean values of resting potential (d), AP amplitude (e), maximal depolarization speed (f), APD50 (g), and APD90 (h) are shown.
Caption: Figure 3: (a) Comparison of atrial APD90 in rabbits with different-intensity continuous training under different Ach + atropine concentrations; (b) comparison of atrial APD90 in rabbits with different-intensity continuous training under different Ach + barium chloride concentrations; (c) comparison of atrial AERP(ms) in rabbits with different-intensity continuous training under different Ach + atropine concentrations; (d) comparison of atrial AERP(ms) in rabbits with different-intensity continuous training under different Ach + barium chloride concentrations.
In both groups, APD90 and APD50 decreased as stimulation frequency increased.
The major findings of our study are as follows: (i) Electrophysiological changes in DM group included prolonged IACT and increased AERPD; (ii) Increased inducibility of AF and LA interstitial fibrosis are evident and may constitute a substrate for the development of AF; (iii) APD90 and APD50 of atrial myocytes were prolonged in diabetic rabbits.
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