The effect of diphenylhydantoin (Dilantin) and quinidine on left ventricular function in dogs

Mierzwiak, Donald S.; Mitchell, Jere H.; Shapiro, William

doi:10.1016/0002-8703(67)90097-x

Cited by 25 publications

(4 citation statements)

References 15 publications

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“…Propyl ene glycol, the solvent for DPH, also has cardiotoxic properties (49). DPH is a negative inotropic agent, although the depression of myocardial function appears to be slight and transient (50)(51)(52). It is also a peripheral vasodila tor-producing hypotension, and may cause central nervous system toxicity ataxia, psychoses, and excitability (50).…”

Section: Antiarrhythmic Drugsmentioning

confidence: 99%

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

Selzer¹,

Cohn²

1970

Annu. Rev. Med.

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Two developments at the beginning of this decade exerted a profound influence upon clinical management of acute myocardial infarction: the in troduction of closed-chest resuscitation with electric shock therapy for ven tricular fibrillation, and the availability of continuous monitoring of the electrocardiogram by means of the cathode-ray oscilloscope. As a result of this, the coronary care unit has become a standard facility for the treatment of myocardial infarction. I t should be recognized that the concept of thera peutic centers for patients with myocardial infarction encompasses a broad range of facilities available in such units (1). On the one end of the spectrum, one can place the comprehensive cardiology center, equipped to treat all as pects and complications of myocardial infarction, including the use of emer gency surgery and artificial pump-support. On the other end, is the small area in a hospital in which nurses can observe the patient's rhythm displayed upon the monitoring oscilloscope. The great majority of coronary care units ap proach the latter end of the spectrum-based primarily on the availability of electrocardiographic monitoring units. Thus, the role of such units is the identification, early recognition, treatment, and prevention of dangerous arrhythmias. The most common arrhythmias that are potentially life-threat ening are related to increased "irritability" of the ventricular myocardium. The purpose of this review is to examine the rationale for the therapy of ventricular arrhythmias in acute myocardial infarction-both the fundamen tal and practical considerations. INCIDENCE OF ARRHYTHMIASDuring the earlier era, when the diagnosis of arrhythmias was based on their occurrence during routine examination of the patient or during record ing of an electrocardiographic tracing, the incidence of arrhythmias was es timated to range between 9 and 27 percent, with an average of 18 percent

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Section: Antiarrhythmic Drugsmentioning

confidence: 99%

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

Selzer¹,

Cohn²

1970

Annu. Rev. Med.

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“…Phenytoin was proposed as an antiairhythmic agent at about the same time as lignocaine but its acceptance as a useful antiarrhythmic drug has been slow. Although the drug has some unique effects on the electrophysiological properties of the heart (Bigger, Schmidt & Kutt, 1968) it also produces myocardial depression (Mierzwiak, Mitchell & Shapiro, 1967;Nayler, McInnes, Swann, Race, Carson & Lowe, 1968) in doses required for therapeutic action (Covino & Shannon, 1969). Several deaths from cardiac arrest and fibrillation have been reported following the use of phenytoin (Mercer & Osborne, 1967;Gellerman & Martinez, 1967;Goldschlager & Karliner, 1967).…”

Section: Introductionmentioning

confidence: 99%

Inotropic actions of lignocaine and phenytoin

Kennedy

Nookhwun

Sadavongvivad

et al. 1971

British J Pharmacology

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Summary1. The inotropic effects of two antiarrhythmic drugs, lignocaine and phenytoin, were studied in electrically driven isolated rabbit atrial preparations. The timeeffect relationship of each drug was investigated with different concentrations and frequencies of stimulation. 2. The effects of time of exposure, drug concentration and heart rate on the development of beat alterations (cessation of beat, skipped beat, alternating variation of force of contraction and extrasystole) were also studied. 3. When the chronotropic effects of both drugs were prevented, the inotropic effects were positive or negative depending on the concentration of drug, time of exposure and frequency of stimulation. 4. At concentrations higher than those obtained in the blood of man on maintenance doses, alteration of the beat occurred but was consistent with the peak blood concentrations immediately after the injection of standard clinical doses. The time of onset of beat alteration shortened when either drug concentration or frequency of stimulation was increased. 5. The beat alteration produced by antiarrhythmic drugs can account for various adverse effects associated with their clinical use. These effects include transient ventricular tachycardia and extrasystole during and shortly after injection of drug, ventricular tachycardia, ventricular fibrillation and cardiac arrest due either to excessive dose or to persistent tachyarrhythmia if the dose is not excessive.

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“…On the other hand, quinidine is generally accepted as an agent which depresses the contractility of the heart (Covino & Shannon, 1969;Goodman & Gilman, 1970;Mierzwiak, Mitchell & Shapiro, 1967;Parmley & Braunwald, 1967). However, a positive inotropic effect of quinidine has also been reported in rat and guinea-pig isolated right atrium (Kruta, 1964), and in a rabbit isolated right atrial preparation suspended in a standard nutrient solution and driven at a low frequency (Kennedy & West, 1969).…”

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confidence: 99%

Effects of Quinidine on Blood Flow Rate and Developed Tension in Blood-Perfused Canine Papillary Muscle

Himori

Taira

1976

Clin Exp Pharmacol Physiol

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1. The effects of quinidine on blood flow rate and developed tension were studied in isolated, blood-perfused papillary muscle preparations of the dog. Drugs were injected into the anterior septal artery. 2. Quinidine caused a dose-related increase in blood flow rate; the mean dose producing a 100% increase in blood flow rate was about 0-3 mg. 3. Quinidine in doses of 0-01-0-1 mg produced a positive inotropic response. With 0-3--1 mg of quinidine the positive inotropic response was preceded by a transient negative inotropic response. With 3 mg there was a monophasic negative inotropic response, the developed tension being reduced by about 40% of control. 4. Propranolol had no statistically significant effects on the responses of the blood flow rate and developed tension caused by quinidine. 5. These results indicate that quinidine has an action on coronary vessels in lower doses than on the myocardium, and that in low doses it has a positive inotropic action rather than the well-known negative inotrophic action exerted with higher doses.

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The effect of diphenylhydantoin (Dilantin) and quinidine on left ventricular function in dogs

Cited by 25 publications

References 15 publications

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

Inotropic actions of lignocaine and phenytoin

Effects of Quinidine on Blood Flow Rate and Developed Tension in Blood-Perfused Canine Papillary Muscle

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