An intermittent infusion of ouabain, 4 mug during 30 sec every 1.5 min, regularly caused ventricular fibrillation in guinea-pigs. The beta-receptor blocking drug, pronethalol (5 mg/kg), increased the dose of ouabain required to produce extrasystoles, completely prevented fibrillation, and significantly raised the lethal dose of ouabain. Dichloroisoprenaline had similar effects, but a dose of 15 mg/kg was required. When fibrillation had already been produced by ouabain, pronethalol (3 to 4 mg) administered slowly restored a regular rhythm, but rapid injection sometimes produced cardiac arrest. As much as 20 to 25 mg/kg of pronethalol could be given to animals deeply anaesthetized with urethane or pentobarbitone, but with light chloroform or ether anaesthesia, 5 mg/kg of pronethalol caused a large fall in blood pressure and complete heart-block.

Anesthetics↗

PubMed1963

A COMPARISON OF THE ANTIFIBRILLATORY ACTIONS AND EFFECTS ON INTRACELLULAR CARDIAC POTENTIALS OF PRONETHALOL, DISOPYRAMIDE AND QUINIDINE.

A quantitative comparison of the effects of quinidine, pronethalol and gamma-di-isopropylamino-alpha-phenyl-alpha-pyrid-2-ylbutyramide (disopyramide) has been made on rabbit isolated atria. All three drugs raised the electrical threshold and reduced the contractions, the conduction velocity and the maximal frequency at which the atria would follow a stimulus. The descending order of potency was pronethalol, quinidine and disopyramide, but the range was small, pronethalol having about twice the activity of disopyramide. Both the new compounds affected intracellular potentials in the same way as quinidine, causing little change in the resting potential or duration of the action potential, but reducing the overshoot potential and slowing the rate of rise of the action potential. These results support the view that interference with depolarization is an essential feature of antifibrillatory activity.

Action Potentials↗

PubMed1963

INHIBITION AND NEUROMUSCULAR PARALYSIS IN ASCARIS LUMBRICOIDES.

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Acetylcholine↗