Synchronization of electrical activity within the atrial tissue was examined by the effect of heptanol on the CV. As shown in Figure 3, the CV recorded from A2 at a distance of 300 |Jm from A1 (key electrode) began to increase over 7 mins after application of heptanol. That is, the CV recorded from A2 was resistant to change induced by heptanol. This indicates that electrical activity is less easily desynchronized within the atrial tissue than within the sinus node, and that gap junctions contribute to synchronization of electrical activities within the atrium.
In the sinus node-atrium preparation experiments, latent pacemaker (follower cell) type action potentials were recorded from the atrial region, and they were well synchronized with action potentials recorded from the sinus node. On impulse propagation between the sinus node and the atrial follower cells, the CV recorded from the atrial follower cells was markedly raised from the beginning of an application of heptanol (Figure 6c). At a lower concentration of heptanol, enhancement of the CV of the atrial follower cells was marked (Figure 6d). This may mean that electrical desynchronization can be most easily induced in the transitional region between the sinus node and the atrial cells.
Figure 6 Changes over time in the coefficient of variation of action potential interval after application of heptanol to (a) sinus node (S1, S2), (b) atrial (A1, A2) and (c) sinoatrial (S-A) preparations. Each point and bar indicate mean ± SEM. *P<0.01 versus S1 (a); versus A1 (b); and versus S (c). d Effect of 0.1 or 0.5 mM heptanol on the coefficient of variation ofS1-S2, A1-A2 and S-A conduction is shown in white portions of columns. The coefficient of variation recorded from key electrodes S1, A1 and S is shown in the black portions of columns. Each column and bar are mean ± SEM. *P<0.01
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