Effects of arrhythmia-producing concentrations of digitoxin on mechanical performance of cat myocardium.
Digitalis toxicity in vivo generally is recognized by the appearance of cardiac arrhythmias but in vitro by a decline in myocardial performance. To determine whether concentrations of digitoxin producing cardiac arrhythmias in intact animals also produce a decline in myocardial performance directly, three groups of adult cats were studied. One received digitoxin daily until arrhythmias developed (toxic group), the second sufficient digitoxin to produce an inotropic effect without arrhythmias (nontoxic group), and the third was untreated. Peak isometric force and maximal dF/dt of isolated right ventricular papillary muscles were significantly greater in nontoxic muscles (3.9 +/- 0.4 gm/mm2 and 21.3 +/- 1.7 gm/mm2 . sec-1). Values in toxic muscles were similar to untreated ones (2.8 +/- -.6 gm/mm2 and 19.0 +/- 3.2 gm/mm2 . sec-1). Acetylstrophanthidin (2 X 10(-8) M) resulted in an increase in peak force and max dF/dt in nontoxic muscles, whereas myocardial performance changed minimally in untreated muscles and declined in 8 of 10 toxic muscles. We conclude that electrical and mechanical toxicity induced by digitoxin frequently coexist.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced*; D002415:Cats; D004074:Digitoxin / Q000008:administration & dosage / Q000494:pharmacology*; D009200:Myocardial Contraction / Q000187:drug effects*; D010210:Papillary Muscles / Q000187:drug effects; D013268:Stimulation, Chemical; D013327:Strophanthidin / Q000031:analogs & derivatives / Q000494:pharmacology
D013327:Strophanthidin; D004074:Digitoxin; C004681:acetylstrophanthidin