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Biomedical subjects

A L Wit

Publications and source records attributed to A L Wit.

At least 109 records · Page 6Linked to original sources
PubMed1975

Electrophysiology and pharmacology of cardiac arrhythmias. VI. Cardiac effects of verapamil.

It is clear from clinical and experimental data that have been reported thus far that verapamil is highly effective in the therapy of cardiac arrhythmias, and that it acts by a different mechanism than most of the commonly used antiarrhythmic drugs. The available clinical data indicate that on intravenous administration verapamil is as good as and perhaps superior to quinidine, procainamide and propranolol for the therapy of many atrial arrhythmias. Unfortunately the extent to which it is useful as longterm prophylaxis has not yet been reported, nor has its toxicity during protracted oral administration. The effects of verapamil on cardiac action potentials clearly indicate that it modifies the slow response to a much greater extent than the fast response. Studies of cardiac tissues from diseased human atria have indicated that slow response action potentials occur frequently. It is possible that such action potentials are responsible for the reentrant and automatic arrhythmias which occur in association with clinical cardiac disease. Whether the efficacy of verapamil in the therapy of atrial arrhythmias is primarily due to abolishing slow response activity in diseased atrial tissues or to suppression of propagation through the atrioventricular node is uncertain. However, it is likely that the therapeutic action of the drug may result from altered propagation of an arrhythmia through the atrioventricular junction as well as from the effects of the drug on diseased atrial and ventricular tissues.

Action Potentials↗
PubMed1975

Time course for reversal of electrophysiological and ultrastructural abnormalities in subendocardial Purkinje fibers surviving extensive myocardial infarction in dogs.

The electrophysiological properties of subendocardial Purkinje fibers surviving in myocardial infarcts were studied with intracellular microelectrodes in isolated superfused preparations and correlated with subsequent light and electron microscopic studies. Transmembrane action potentials could always be recorded from one or two cell layers of subendocardial Purkinje fibers in infarcted regions 3 days to 7 weeks after coronary artery occlusion; ventricular muscle action potentials were rarely found. Microscopic studies also demonstrated several layers of intact subendocardial Purkinje fibers; the subjacent ventricular muscle cells were irreversibly injured and replaced by scar. At all time intervals, surviving Purkinje fibers had significantly reduced maximum diastolic potentials, action potential amplitudes, and depolarization velocities as well as prolonged action potential durations. These parameters normalized between 24 hours and 7 weeks after coronary artery occlusion. Surviving Purkinje fibers with electrophysiological abnormalities at 24 hours and 3 days contained vast lipid deposits. Lipid was less prevalent at 10 days when action potential characteristics had improved. By 7 weeks, action potentials were nearly normal and lipid was absent. Subendocardial Purkinje fibers surviving in infarcts are subject to conditions which cause electrophysiological and ultrastructural abnormalities. Persistent abnormalities in the electrophysiological properties of these surviving Purkinje fibers may cause persistent altered electrophysiological properties of the infarcted heart.

Action Potentials↗
PubMed1975

Possible electrophysiological mechanisms for lethal arrhythmias accompanying myocardial ischemia and infarction.

Ventricular arrhythmias are probably the cause of sudden death due to myocardial ischemia or infarction. Such arrhythmias result from alterations in the transmembrane potentials of ventricular muscle and Purkinje fibers. Most of our knowledge concerning mechanisms for these arrhythmias has been derived from experimental studies on the canine heart. In this model, the early ventricular arrhythmias which occur within minutes after coronary artery occlusion probably have different electrophysiological mechanisms than the late arrhythmias which occur several or more hours after the onset of ischemia. The early arrhythmias probably result from reentry in ventricular muscle due to slow conduction in ischemic or infarcting muscle cells. The later arrhythmias most likely arise in subendocardial Purkinje fibers which develop spontaneous diastolic depolarization and abnormally prolonged action potential duration. It is important for future investigations to determine the relevance of electrophysiological studies on the canine heart to human ischemic and infarction arrhythmias.

Action Potentials↗