We studied the role of acetylcholine (ACh) and calcium overload in the indu
ction of atrial flutter or atrial fibrillation (AF) in right atria from 34
normal male Syrian hamsters (F1B) and 33 cardiomyopathic Syrian hamsters (B
IO 14.6) associated with focal myocardial necrosis. Action potential (AP) w
as recorded with conventional microelectrode techniques and twitch force by
a transducer. ACh (0.1, 1 and 10 mu M) induced high-frequency AF (around 3
3 Hz) along with tension oscillations and contracture in 7 of 12 normal ham
ster atria, These effects of ACh were abolished by tetrodotoxin or quinidin
e as well as by atropine, In contrast, ACh induced AF only in 1 of 12 myopa
thic atria, In both normal and myopathic atria, ACh induced similar changes
in AP duration, spontaneous rate and force. The effects of calcium overloa
d were tested by means of a high [Ca2+](o) (8.1 mM) low [K+](o) (1 mM) solu
tion in another series of experiments. This solution also induced incidence
of AF higher in normal (10/12) than in myopathic atria (4/12). The calcium
load was also increased by high-frequency pacing (32 Hz for 3 or 30 s): AF
occurred in normal atria (5/8), but not in myopathic atria (0/8). Measurem
ent of the refractory period revealed a longer refractory period in myopath
ic than in control atria. We concluded that the lower incidence of AF in my
opathic atria was probably due to their longer refractory period and the as
sociated focal myocardial necrosis which then hindered the establishment of
such a reentrant rhythm.