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AJP - Heart and Circulatory Physiology, Vol 252, Issue 3 645-H652, Copyright © 1987 by American Physiological Society
ARTICLES |
R. M. Terek and C. T. January
Oscillatory afterpotentials, or late afterdepolarizations, are one mechanism postulated to cause cardiac arrhythmias and possibly conduction disturbances. We studied excitability by determining strength-interval curves in Purkinje fibers under normal conditions and during the presence of oscillatory afterpotentials induced by cardiac glycoside toxicity. During exposure to acetylstrophanthidin (0.10-0.15 mg/l), the mean resting potential depolarized 5.6 mV and oscillatory afterpotentials of 3-17 mV appeared. Current threshold for evoking action potentials was reduced below control level (e.g., increased excitability) throughout electrical diastole. Associated with oscillatory afterpotentials was a marked biphasic variation in current threshold giving strength-interval curves a characteristic biphasic shape. During the rising phase of the oscillatory afterpotentials, excitability reached a maximum, whereas the minimum increase in excitability occurred during the falling phase of oscillatory afterpotentials. This biphasic change in excitability remained correlated with the oscillatory afterpotentials at different cycle lengths. Results show that during acetylstrophanthidin toxicity excitability is increased throughout electrical diastole, and characteristic time-dependent changes in excitability occur during oscillatory afterpotentials. Time-dependent changes in excitability were detected with both intra- and extracellular stimulation techniques.
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