Abstract

Hypermagnesemia occurs in elderly people or patients with renal insufficiency after excessive ingestion of magnesium-containing laxatives. In addition to typical electrocardiogram (ECG) findings caused by conduction defects, changes in the ST segments and T waves are also observed in patients with severe hypermagnesemia. This suggested the involvement of similar pathophysiology to acute myocardial infarction, as we previously demonstrated using burn-induced subepicardial injury model in frog hearts. In the present study, by exposing the bullfrog heart to high-magnesium solution, we reproduced prominent ST segment changes in ECG as actually observed in patients with severe hypermagnesemia. In addition to the great increase in the T waves, the ECG showed a marked elevation of the ST segments and the cardiac action potential demonstrated a marked shift of the resting membrane potential to the depolarized side. High-magnesium exposure did not affect the abundance of Na+/K+-ATPase proteins. However, the pharmacological stimulation of Na+/K+-ATPase activity by insulin quickly retrieved the elevated ST segments in ECG. From these results, the functional blockade of Na+/K+-ATPase activity by magnesium ions was thought to be responsible for generating the potassium concentration gradient and the subsequent ST segment changes.

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