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At least 379 records · Page 21Linked to original sources
PubMed1983

Use of heart cell cultures as a tool for the evaluation of halothane arrhythmia.

The effects of various combinations of epinephrine-halothane and epinephrine-enflurane were tested on beating myocardial muscle cells cultured from 2- to 3-day-old rats. A series of culture plates containing myocytes were exposed to 0.5, 1.0, 1.5, and 2% halothane. At each halothane concentration, 9 ng of epinephrine was added, and the rate of contraction and rhythm of myocytes were observed. With increasing halothane concentrations, a significant and progressive increase in the percentage of plates demonstrating arrhythmia was observed. In a separate series of experiments, doses of epinephrine were added following exposure to 1.5% halothane. As the dose of epinephrine was increased progressively more plates displayed arrhythmia. In addition, culture plates were exposed to enflurane (3 and 6%), and epinephrine was added to each plate. No arrhythmia was observed in any of the 3% enflurane exposed plates. However at 6%, 100% of the plates displayed arrhythmia. In another series of experiments the efficaciousness of quinidine, procaine amide, lidocaine, propranolol, and verapamil in converting cell culture arrhythmia to normal rhythm following epinephrine and halothane was tested. Quinidine converted 96% of all arrhythmic plates to normal rhythm, procaine amide 80%, lidocaine 50%, and propranolol 10%. Verapamil failed to convert any arrhythmic plates to normal rhythm. It was concluded from this study that halothane directly "sensitizes" heart cells in tissue culture, and that the "sensitization" process is a linear, dose-dependent phenomenon.

Action Potentials↗
PubMed1978

Some effects of disopyramide and its N-dealkylated metabolite on isolated nerve and cardiac muscle.

In animals and man the antidysrhythmic agent disopyramide in primarily metabolised by mono-N-dealkylation. The effects of disopyramide and its N-dealkylated metabolite (MIP) have been investigated using isolated cardiac and nervous tissue, and their effects have been compared with the effects of other antidysrhythmic agents. Disopyramide, d,l-propranolol and quinidine all decreased both maximum driving frequency and developed tension in electrically driven guinea pit atria. MIP and procaine amide also decreased maximum driving frequency, but had a positive intropic effect. MIP was only 4 times less active than disopyramide in decreasing maximum driving frequency. There was no evidence that either disopyramide or MIP possessed beta-adrenoceptor antagonist properties. In superfused rat sciatic nerves, it has been shown that neither disopyramide nor MIP possesses significant local anaesthetic properties. Procaine amide and lignocaine were highly active in this test. The possible contribution of MIP to the actions of disopyramide in vivo is discussed.

Action Potentials↗
PubMedDate not supplied

[Structural rearrangements in membranes induced by anesthetics].

Studies were carried out on the effects of anesthetics on the stability of membranes to sodium dodecylsulfate and trypsin. The initial rate of membrane desintegration by detergent evaluated by light scattering with stopped flow method was increased in the presence of ethanol, propanol, benzyl alcohol, procain-amide (erthrocyte membrane) and chlorpromazine (rat brain synaptosomes). Concentrations of anesthetics which correspond to half of the maximum effect were very close to that of blocking the action potential and inducing 50%--antihemolysis. Alcohols and procaine at anesthetic concentrations inhibited proteolysis of isolated erythrocyte membranes but were without effect on their ultrasonic fragments. Increase of membrane desintegtation rate is interpreted as structural rearrangements of membranes with the weakening of detergent sensitive intermolecular interactions. Proteolysis inhibition of ghosts but not the gragments indicates against the participation of the basic func of proteins in the structural membrane rearrangements.

1-Propanol↗
PubMed1975

Mechanism of frequency-dependent inhibition of sodium currents in frog myelinated nerve by the lidocaine derivative GEA.

A new lidocaine derivative (Astra, GEA 968) depresses excitability of myelinated frog nerve in a manner which depends upon the rate of use of the nerve. This phenomenon has been shown, under voltage clamp conditions, to involve "frequency-" or "use-dependent" inhibition of the transient inward sodium currents at the node of Ranvier. With 0.6 mM GEA 968 in the solution bathing the node, the inward sodium currents produced by 5-msec depolarizing pulses to -20 mV are reduced to 40% of control values if the node is rested for a few hundred seconds prior to the test pulse. Repetitive opening of the sodium channels by depolarizing pulses enhances this inhibition, for example, currents are eventually reduced to 10 to 20% of control with repetitive depolarization at 2 sec-1. If the preparation is then allowed to rest, this use-dependent increment in inhibition gradually declines with a time constant of about 10 seconds. Repetitive opening of the sodium channels by depolarizing pulses preceded by large hyperpolarizing prepulses reverses the inhibition caused by application of depolarizing pulses alone. It is hypothesized that the GEA 968 molecule binds to open sodium channels and, in doing so, simultaneously blocks the channel and shifts the curve relating sodium inactivation to membrane potential by 20 to 40 mV in the hyperpolarizing direction. Several kinds of evidence supporting this molecular hypothesis are presented. Lidocaine, procaine, procaine amide and a quaternary lidocaine derivative QX-314 also cause use-dependent depression of sodium currents in this preparation. This common mode of action of tertiary and quaternary anesthetics implies that the cationic form of tertiary anesthetics is active.

Animals↗
PubMed1975

Sustained accelerated idioventricular rhythm.

A 73-year-old white man became easily fatigued and hypotensive six weeks after a documented acute inferior myocardial infarction. Continuous ECG monitoring showed a sustained tachycardia with a right bundle branch block pattern. A His bundle electrogram showed no His deflection prior to ventricular activation. The patient was successfully treated with intravenous procaine amide resulting in reversion to sinus rhythm, loss of symptoms, and return of blood pressure to normal levels. The unique aspects of this case and therapeutic considerations in the management of this problem are discussed.

Aged↗
PubMed1975

Coronary artery surgery for recurrent ventricular arrhythmias in patients with variant angina.

Two patients with Prinzmetal's variant angina had recurrent episodes of resting chest pain, ST segment elevation, QRS widening, ventricular tachycardia, and ventricular fibrillation. These eqisodes were unresponsive to medical therapy including lidocaine, procaine amide, and quinidine sulfate. Coronary arteriography revealed severe obstructive coronary artery disease, involving more than one coronary artery, in both patients. Aorticocoronary saphenous vein grafts were utilized to bypass significant disease in each patient. In one patient blood flow through the grafts was measured at 90 and 65 ml per minute, respectively, at operation and patent grafts were demonstrated six months postoperatively. Neither patient has had recurrence of chest pain or evidence of ventricular tachycardia at one year or 2 1/2 years postoperatively. Postoperative resting and maximal exercise ECG's are normal. Coronary artery surgery may be an effective method of therapy for ischemic ventricular tachycardia when medical therapy fails.

Adult↗
PubMed1979

Effects of some antiarrhythmic agents on dog heart mitochondrial oxidative phosphorylation.

Significant decreases in state 3 oxygen consumption, respiratory control index (RCI), ADP : O ratio and phosphorylation rate were observed in the presence of 0.1-1.0 mM quinidine; 0.5 mM or greater concentrations elevated state 4 oxygen consumption. Lidocaine (1-2.5 mM) also depressed RCI and increased state 4 oxygen consumption but procaine amide (1-2.5 mM) was without effect. It is suggested that cardiodepression by quinidine may be associated with its ability to impair mitochondrial metabolism.

Adenosine Diphosphate↗
PubMed1977

In vivo atrial excitability and anti-arrhythmic drugs.

The threshold of excitability of the atrial muscle was studied in the in vivo beating canine heart. Unipolar cathodal and anodal strength-interval curves were constructed and found to be dissimilar in shape. It was found that at any interval within the relative refractory period of the atrium, as in the ventricle, there is a wide range of current levels delineated by an upper (TU) and lower (TL) limit of threshold which can stimulate the atrial myocardium. Within these limits the threshold varies spontaneously and can be reduced to TL level by a run of extrasystoles. Such TU and TL curves were repeatedly determined following administration of therapeutic doses of quinidine, procaine amide or lidocaine. It was observed that all three drugs prolonged the refractory period. The TU values increased following each of the drugs, and mostly after quinidine, while the TL curve was less affected by quinidine. It is suggested that the exit block thus produced is the principal mechanism whereby quinidine depresses atrial disrhythmias.

Animals↗
PubMed1980

Ventricular tachyarrhythmias in regional myocardial hyperkalemia: efficacy of three antiarrhythmic agents.

Potassium chloride infusion into the left anterior descending coronary artery induces a sequence of events analogous to those occurring during acute transmural ischemia. These include ST elevation, intramural conduction delay, ventricular techyarrhythmias and fibrillation. The influence of antiarrhythmic agents in an intact anesthetized canine model have not previously been tested. We have evaluated the efficacy of lidocaine, procaine amide and practolol in animals during regional hyperkalemia. In the untreated, only 9% survided a 20 minute observation period. All three treatment groups exhibited a reduced incidence of tachycardia and 74% survived the test period. In each treatment group this was associated with a further prolongation of intramural conduction time in the affected wall. This antiarrhythmic efficacy, thought possibly to be due to transformation of unidirectional to bidirectional block, supports the view that modulation of transcellular potassium activity contributes to the control of ischemic arrhythmias.

Animals↗
PubMed1981

Respiratory and vagal modulation of ventricular tachycardia.

This is a report of a case of stable uninterrupted spontaneous ventricular tachycardia which could be temporarily terminated by a strong increase in vagal tone reflexly induced by phenylephrine, 0.2 mg I.V. Following its abolition with procaine amide, 100 mg I.V., ventricular tachycardia was found to be reinducible by deep inspiration for limited periods of time which varied directly with the magnitude of the inspiratory volume. This effect was enhanced by vagal inhibition (atropine, 0.6 mg I.V.) and attenuated or prevented by vagal stimulation (carotid sinus massage or edrophonium 10 mg I.V.). It was concluded that a deep inspiration can, under some circumstances, induce ventricular tachycardia by a mechanism of vagal withdrawal.

Dose-Response Relationship, Drug↗