Date of Defense

Spring 4-18-2003

Department

Biological Sciences

First Advisor

William F. Jackson, Biological Sciences

Second Advisor

John Jellies, Biological Sciences

Third Advisor

John Spitsbergen, Biological Sciences

Abstract

Cardiotoxicity is prevalent among pharmaceuticals that possess the ability to block cardiac K+ channels. During a single cardiac cycle, the contributions of Na+, K+, and Ca++ currents determine the duration of the action potential. The transient outward K+ current Ito, provide K+ efflux during the beginning phases of the cardiac action potential, while the rapid component of the delayed rectifier K+ current, IKr, provides K+ efflux during the mid-to-late phases. Quinidine and 4-aminopyridine, well known for their abilities to block K+ channels and prolong action potential duration, target IKr and Ito, respectively. These agents are known to block these currents in other cardiac models and thus serve as standards in which to judge the efficacy of an animal model. Little is known about the electrophysiology of the hamster right atrium. The aim of this study was to assess the abilities of quinidine and 4-aminopyridine prolonged both APD50 and APD90, while quinidine also reduced heart rate. These results suggest that hamster right atrial myocytes possess the ion channels contributing to Ito and IKr. Thus, the hamster model may be useful in future testing of the cardiotoxic effects of pharmaceuticals.

Access Setting

Honors Thesis-Campus Only

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