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Lanthanum of 0.1 to 0.2 mM caused a twitch inhibition and further showed a marked, long-lasting twitch potentiation during washout in both ventricular strips of bullfrog and atrial or papillary muscles of guinea-pig. It was found that the effect was more conspicuous in the frog heart. A similar potentiation was observed by applying gadolinium instead of lanthanum. The participation of endogeneous catecholamine release is unlikely since the positive inotropic effect was never affected by the presence of beta-adrenergic blocker. The potentiation was not accompanied by any increase in the action potential plateau, suggesting independence of the phenomenon on the calcium current. A marked elevation of the resting tension was produced during a long-term lanthanum perfusion, reflecting the increase in the intracellular calcium level. On the other hand, transient increase in the resting tension was frequently observed on returning to normal Ringer solution. The latter change seemed to result from a transient increase in the resting permeability to calcium ions. The negative or positive inotropic effect by increasing or lowering the external sodium concentration observed under the control condition was strongly depressed during the twitch potentiation. In addition, sodium-free contracture induced by solutions isotonically replaced with sucrose or potassium chloride was augmented both during lanthanum perfusion and during its washout. These results suggest the possibility that the elevation of the intracellular calcium level due to inhibition of Na-Ca exchange mechanism and/or increase in the calcium permeability is the principal cause for the twitch potentiation caused by lanthanum washout.

Paradoxical after-potentiation of the myocardial contractility by lanthanum.