Rate and rhythm dependency of propagation from normal myocardium to a Ba++, K+-induced slow response zone in rabbit left atrium.

Strips of rabbit atrium 2-3 mm wide and 10-12 mm long were used to study how normal propagating action potentials excite a region where slow responses are the only form of electrical activity. One end of the preparation was bathed in normal Tyrode's solution. The rest was exposed to Tyrode's solution with high K+ (12.7 mM) and Ba++ (1 mM) (TKBa solution). The normal end was electrically stimulated and activity was monitored extra- and intracellularly (3 M KCl microelectrodes) as it propagated into the TKBa-treated region. We observed that the slow response could be elicited optimally by the normal action potential only within a limited range of stimulation frequencies (from around 0.3 to 1 Hz). At higher frequencies, progressive "fatigue" of slow response was observed. At frequencies lower than this range, normal action potentials were unable to stimulate slow response. To clarify the mechanism under this behavior, slow responses were directly elicited by electrical stimulation of strips wholly bathed in TKBa. Rate dependency of slow response excitability was again observed. Conclusions are: slow response excitability is enhanced transiently at each stimulation; the enhanced excitability state subsides very slowly and may take as long as 10 seconds to disappear; the enhanced state is cumulative from cycle to cycle so that excitability increases with increasing frequencies of stimulation above 0.1 Hz; and high frequency block due to fatigue and block due to excitability depression at low frequency delimit an optimal frequency window for slow response excitation and conduction.