Abstract

AbstractVerapamil (1 μg/ml) completely abolished a population of markedly depressed action potentials of cells (BZ-1) in border zones around healed infarcts. Even at higher concentrations, verapamil had no such inhibitory effect on other border zone cells (BZ-2), normal and central infarct zones cells. BZ-1 cells demonstrated a severely depressed Vmax (<20 V/sec), accompanied by partial depolarization, while BZ-2 cells were characterized by abbreviated duration. Verapamil only significantly depressed Vmax of BZ-1 cells. Action potential amplitude and action potential duration at 50% repolarization of all cells were abbreviated by verapamil. These results indicate slow inward currents may be involved in the genesis of action potentials in BZ-1 cells.

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