Electrical and ionic mechanisms of early reperfusion arrhythmias in sheep cardiac Purkinje's fibers

Abstract

The mechanisms of induction of early reperfusion arrhythmias were studied in sheep cardiac Purkinje's fibers superfused in vitro. Transmembrane potentials, intracellular sodium activity (a i Na), and contractile force were recorded. Stoppage of the flow of Tyrode's solution (ischemia) for 1 hour initially decreased slightly a i Na (−0.57 mmol −7.2%), increased the action potential amplitude (+6.1%) and duration (+7.8%), and decreased diastolic depolarization slope (−45.2%). As the ischemia continued, a i Na increased progressively (to 12.53 mmol, +56.2%), whereas force peaked (+395%) after about 30 minutes and then began to decrease. By the end of ischemia, there was a decrease in action potential amplitude (−14.9%) and duration (−39.6%), whereas diastolic depolarization slope reincreased again almost to control value (−7%). When the flow of Tyrode's solution was resumed (reperfusion), force markedly increased (+211.1%) and oscillatory potentials initiated arrhythmias (extrasystoles and repetitive fast discharge) in 64% of tests. Force and a i Na decreased relatively rapidly. The arrhythmias initiated after 58.4 ± 1.8 seconds of reperfusion and lasted 101.5 ± 3.2 seconds. When [Na] o was increased by +19.2%, reperfusion arrhythmias occurred after only 30 minutes of ischemia. Thus, in Purkinje's fibers superfused in vitro, early reperfusion arrhythmias are induced by oscillatory potentials caused by calcium overload, which is enhanced by the increase in a i Na during ischemia.