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Biomedical subjects

J C Bailey

Publications and source records attributed to J C Bailey.

At least 55 records · Page 3Linked to original sources

Differences between proximal left and right bundle branch block action potential durations and refractoriness in the dog heart.

To date the electrophysiological mechanism responsible for aberrant intraventricular conduction of critically timed premature supraventricular impulses has not been documented. Microelectrode techniques were used to measure in vitro action potential and refractory period durations of the canine proximal right and left bundle branches equidistant from the distal bundle of His. Both measurements in the right bundle branch were statistically significantly longer than these parameters of the left bundle branch. Transection of the bundle branches immediately distal to the distalmost recording sites effected no change in the proximal right bundle action potential but caused marked prolongation of proximal left bundle branch action potential and refractory period durations. We conclude that functional right bundle branch aberrancy is most likely due to the longer proximal right bundle action potential duration and refractoriness. Our data also suggest that the shorter proximal left bundle branch action potential durations and refractory periods may be due to the proximity of the low ohmic resistance Purkinje fiber-muscle junctions on the left septal surface, effecting electrotonic foreshortening of these proximal left bundle branch parameters.

Action Potentials↗

Electrophysiological observations on the digitalis-potassium interaction in canine Purkinje fibers.

We studied the effects of elevating potassium concentration on the membrane potential of Purkinje cells exposed to toxic concentrations of acetylstrophanthidin or ouabain. Conventional intracellular microelectrode techniques were employed. Rapid elevation of [K+]o from 2.7 to 5.4 mEq/liter resulted in an initial increase (more negative) in membrane potential of cells demonstrating ouabain-induced phase 4 depolarization. The increase in maximal diastolic potential occurred initially without suppression of phase 4 depolarization. In cells rendered inexcitable by ouabain or acetylstrophanthidin, elevation of [K+]o consistently increased membrane potential and restored excitability. In four experiments automaticity was initiated within 2 minutes after the increase in [K]o. Although automaticity reappeared, as maximal diastolic potential increased, the automatic rate slowed and then pacemaker activity was suppressed. Studies with 3H-ouabain showed that the increase in membrane potential paralleled K+-induced release of 3H-ouabain from Purkinje cells. These studies suggest that elevation of [K+]o reverses digitalis toxic manifestations in canine Purkinje fibers by causing release of cardiac glycosides bound to the membrane. The observed increase in membrane potential of ouabain-treated Purkinje fibers that occurred after [K+]o elevation was considered to be mediated in part by restoration of the Na pump and by electrogenic pumping.

Action Potentials↗

Ventricular echoes.

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Arrhythmias, Cardiac↗