In anesthetized dogs treated with ouabain, the ventricular escape intervals were measured after (1) vagally induced atrioventricular block, (2) ventricular premature stimulation, or (3) cessation of a period of regular pacing at various cycle lengths. The escape intervals were a direct function of the basic cycle length and were significantly influenced by the last cycle length, whether premature or postmature. Postpacing acceleration of atrial ectopic responses was also demonstrated. When compared with results obtained in isolated Purkinje tissue, ectopic activity associated with early ouabain toxicity appears to be caused by frequency-related transient depolarizations rather than "true" phase 4 depolarization.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine