The mechanism of
bradycardia caused by the administration of
succinylcholine has not been fully elucidated. Accordingly, the effects of
succinylcholine and
succinylmonocholine on the sinoatrial node were studied in 35 mongrel dogs. The sinus node artery was selectively perfused with autologous blood from a femoral artery at a constant pressure of 100 mmHg, and 30 to 1,000 micrograms of
succinylcholine or
succinylmonocholine was administered directly into the artery.
Succinylcholine caused a transient (63-600 s) dose-related positive chronotropic effect. The heart rate was increased to 14.4 +/- 2.1% (mean +/- SE) above the control value after the administration of 1,000 micrograms of
succinylcholine. This positive chronotropic effect was inhibited by pretreatment with
pindolol or
reserpine. By contrast,
succinylmonocholine produced a transient (30-248 s) dose-related negative chronotropic effect. The heart rate was decreased to 17.5 +/- 1.4% below the control value after administration of 1,000 micrograms of
succinylmonocholine. The negative chronotropic effect was blocked partially by
atropine. It was concluded that the positive chronotropic effect of
succinylcholine may be mediated through
beta-adrenergic receptor stimulation by
catecholamine released from the
adrenergic nerve endings in the sinoatrial node, and that the negative chronotropic effect of
succinylmonocholine may be the result of excitation of
cholinergic receptors in the sinus node. However, a direct effect of
succinylmonocholine on the sinus node could not be ruled out.