Chronotropic effects of succinylcholine and succinylmonocholine on the sinoatrial node.

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.