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 ± 8.2% decrease occurred (P < 0.01). H-V time showed no change (from 30 ± 2.7 to 31.5 ± 2.4 ms) at the onset of toxicity but after toxicity, it lengthened to 40.5 ± 3.1 ms (P < 0.05). QRS did show significant prolongation (69.5% ± 5.3 to 79.5 ± 6.9 ms; P < 0.05) at the onset of toxicity, but this was more marked (79.5 ± 6.9 to 130.5 ± 8.1 ms; P<0.01) after toxicity. H-S time was significantly prolonged (99.5 ± 6.2 to 111.0 ± 8.9 ms) before (P < 0.02) and after (P < 0.01) toxicity (111.O ± 8.9 to 171.1 ± 10.6 ms). During toxicity there is progressive increase in contractile force with continued ouabain infusion. Progressive prolongation of intramyocardial conduction occurs in nontoxic and toxic doses, but His-Purkinje conduction is prolonged only in supratoxic doses.