Cardiovascular Research, 1975, 9, 65-12.
Contractile and electrophysiological responses to progressive digitalis t oxicity1 v . s.
BANKA, B. J . SCHERLAG,
and
R. H . HELFANT
From the Division of Cardiology, Presbyterian-University of Pennsyhania Medical Center, 51 North 39th Street, Philadelphia, Pennsylvania 19104, U S A
Contractile force and intraventricular conduction during progressive ouabain infusion were examined in 15 dogs using a Walton-Brodie strain gauge arch and sequential atrial and bundle of His pacing. This permitted: (1) contractile force determination; (2) overdrive of arrhythmias; (3) maintenance of normal contraction sequences ; (4) ‘ normal’ ventricular depolarization; (5) rate control ; (6) conduction measurements of the H-V interval (His-Purkinje conduction), QRS (intramyocardial conduction), and H-S interval (total intraventricular conduction). Contractile force increased 21.2+4.3% at the onset of toxicity. After toxicity, there was a significant further increase (P < 0.01) to 50.1 f 12.4%. However, immediately before ventricular fibrillation, a 43.8 f 8.2% decrease occurred (P < 0.01). H-V time showed no change (from 30 f 2.7 to 31.5 k 2.4 ms) at the onset of toxicity but after toxicity, it lengthened to 40.5k3.1 ms (P
Contractile and electrophysiological responses to progressive digitalis t oxicity1 v . s.
BANKA, B. J . SCHERLAG,
and
R. H . HELFANT
From the Division of Cardiology, Presbyterian-University of Pennsyhania Medical Center, 51 North 39th Street, Philadelphia, Pennsylvania 19104, U S A
Contractile force and intraventricular conduction during progressive ouabain infusion were examined in 15 dogs using a Walton-Brodie strain gauge arch and sequential atrial and bundle of His pacing. This permitted: (1) contractile force determination; (2) overdrive of arrhythmias; (3) maintenance of normal contraction sequences ; (4) ‘ normal’ ventricular depolarization; (5) rate control ; (6) conduction measurements of the H-V interval (His-Purkinje conduction), QRS (intramyocardial conduction), and H-S interval (total intraventricular conduction). Contractile force increased 21.2+4.3% at the onset of toxicity. After toxicity, there was a significant further increase (P < 0.01) to 50.1 f 12.4%. However, immediately before ventricular fibrillation, a 43.8 f 8.2% decrease occurred (P < 0.01). H-V time showed no change (from 30 f 2.7 to 31.5 k 2.4 ms) at the onset of toxicity but after toxicity, it lengthened to 40.5k3.1 ms (P
