Effect of Quinidine and Pronethalol on Acetylstrophanthidin-Induced Ventricular Arrhythmia in Cats Treated with Reserpine

Levitt, Barrie; Roberts, Jay

doi:10.1161/01.res.19.3.622

Cited by 24 publications

(7 citation statements)

References 16 publications

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“…Pretreatment of the normal dogs with reserpine increased the lethal dose of ouabain by about 20% whereas both dicliloroisoproterenol and pronelhalol increased it by 30 to 34% of the control value. These results are in agreement with the obser-vat ion that reserpine and /^-adrenergic receptor blocking agents prevent the arrhythmias induced by cardiac glycosides [8,9,11,13,17]. 1 Reserpine (0.5 mg/kg i.p.)…”

Section: Methodssupporting

confidence: 88%

“…In contrast, Levitt and Roberts [8] did not observe such an action of pronethalol in reserpine-pretreated cals. This discrepancy may be due to either species dif ference or to the very high dose of reserpine (5 mg/kg) used by these investigators.…”

Section: Resultsmentioning

confidence: 76%

“…17], While we were studying whether or not pronetlialol and reserpine produce antiarrhythmic action through similar mechnisms, two conflict ing reports appeared in the literature. Levitt and Roberts [8] showed that in reserpine-treated cats, pronetlialol failed to increase the dose of acetylstrophanthidine, which induced arrhythmia in combination with vagal stimulation. On the other hand, Tuttle and In n e s [18J demonstrated that pronetlialol converted ouabaininduced arrhythmias to sinus rhythm in dogs pretreated with reserpine.…”

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confidence: 99%

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Influence of Pronethalol on Ouabain Toxicity in Dogs Treated with Reserpine

Dhalla¹,

Bhagat²

1968

Cardiology

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Section: Methodssupporting

confidence: 88%

Section: Resultsmentioning

confidence: 76%

mentioning

confidence: 99%

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Influence of Pronethalol on Ouabain Toxicity in Dogs Treated with Reserpine

Dhalla¹,

Bhagat²

1968

Cardiology

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“…A similar quantitative antiarrhythmic difference between the isomers of propranolol was observed against ouabain induced toxicity in cats and dogs (13). From these results it appears that the an,tiarrhythmic activity exerted by dexpropranolol is due lto the quinidine-like or local anesthetic properties common to many of the isomers of beta adrenergic blocking compounds.…”

Section: ( -)supporting

confidence: 59%

Effect of Various Antiarrhythmic Drugs on the Daunomycin-Induced Arrhythmia in the Hamster

Herman¹,

Schein²,

Taylor³

et al. 1970

Experimental Biology and Medicine

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Daunomycin 151), an antibiotic, has been found to acutely induce a bidirectional ventricular arrhythmia in the hamster ( 1 ) . Arrhythmias have also been induced experimentally following ouabain (2), ligation of the anterior descending coronary artery (3), administration of epinephrine during cyclopropane anesthesia (4) or hypothermia (5). Numerous studies have shown that these arrhythmias can be suppr.essed by various types of drugs including beta adrenergic blocking compounds. The present study was initiated to determine to what extent the daunomycin arrhythmias in the hamster are modified by antiarrhythmic drugs.Methods and Materials. Male golden hamsters weighing between 90 ,to 140 g were used in all experiments. Anesthesia was induced with an intraperitoneal (ip) injection of 45 mg/kg of sodium pentobarbital (Nembutal) . A standard lead I1 electrocardiogram (ECG) was monitored from needle electrodes inserted into the appropriate limbs and hear't rate was determined by means of a cardiotachometer. In some experiments, right carotid artery blood pressure was monitored through a Sanborn 267B transducer and respiratory movements were detected by means of a differential pressure transducer attached to a tracheal cannula. All parameters were recorded with a Hewlett-Packard polygraph.Each hamster was administered 50 mg/kg of daunomycin. A supplemental dose of 25 mg/kg was'then given if the ECG pattern did not become abnormal within 15 min. The challenge agents or saline were given over a Supported in part by Contract PH43-68-2283 from Chemotherapy, National Cancer Institute, NIH.2-min period when the arrhythmia had been established for 5 min. The onset and duration of any antiarrhythmic activity were recorded. Heart rates were determined prior to daunomycin, prior to and following test drug administration. Experiments were terminated 30 min following test drug administration.Drugs, calculated as the free base, were dissolved in physiological saline prior to the beginning of each experiment. Injections were made through a fermoral vein cannula in a dose volume of 0.1-0.2 ml followed by a 0.2-ml saline wash.The compounds studied and doses (mg/kg ) were : dl-propranolol hydrochloride (Inderal) (0.25, 0.5, 1.0, and 2.0), d-propranolol hydrochloride ( 1 .O, 2.0, and 4.0) , diphenylhydantoin sodium (Dilantin) ( 12.5 and 25.0), quinidine sulfate, (1.5, 3.0, and 6.0) procainamide hydrochloride ( Pronestyl) 1.2, 6.0, and 20.0), lidocaine hydrochloride (Xylocaine) (1.0, 5.0, and 10.0) dZ-[4-2 ( -isopropylamino-1 -hydroxyethyl) methanesulfonanilide hydrochloride] (dl-M J 1999) (1, 3, and 6.2)) and ~(-)-l-N-isopropyl-P-nitrophenyl-ethanolamine hydrochloride D (-)

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“…Although the sinus slowing shows that the countershock stimulates parasympathetic fibers, it seems reasonable to assume that countershock stimulates both sympathetic and parasympathetic components of peripheral autonomic nerves. Because of the known relationships between the actions of digitalis and those of norepinephrine (2)(3)(4)(5)(6)(7)(8) and because of evidence that digitalis inhibits the uptake of norepinephrine by various tissues (9)(10)(11) we decided to test the hypothesis that arrhythmias observed immediately after exposure of a digitalized patient to countershock are due in part to the liberation of norepinephrine from nerve terminals by the electrical pulse, and in part to altered release or uptake of norepinephrine by the nerve fibers resulting from the action of digitalis on the nerve membrane or both. These 376 TEN EICK, WYTE, ROSS, HOFFMAN events would increase the time of exposure of cardiac tissue to catecholamine as well as the mean concentration of amine following a single countershock; under the influence of digitalis, certain cardiac fibers might respond to this condition by developing arrhythmias (12,13).…”

mentioning

confidence: 99%

Post-Countershock Arrhythmias in Untreated and Digitalized Dogs

Eick

Wyte

Ross

et al. 1967

Circulation Research

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Recent studies suggest that countershock can stimulate cardiac autonomic nerves and that the resulting release of norepinephrine contributes to postcountershock (PCS) arrhythmias. /J-Adrenergic receptor blocking agents, reserpine, cocaine, and cardiac-denervated preparations were used to evaluate this hypothesis in dogs under pentobarbital anesthesia. The suitability of the dog as an experimental system was examined. In the normal dog, the duration of PCS arrhythmia caused by a countershock of given energy was increased 100% by ouabain (0.05 mg/kg iv). In both normal dogs and dogs given ouabain (0.05 mg/kg iv), dicbloroisoproterenol, pronethalol, and propranolol reduced the duration of PCS arrhythmia; reserpine, a norepinephrine depletor, reduced the duration of PCS arrhythmia; cocaine, a norepinephrine-uptake inhibitor possessing antiarrhythmic properties, increased the duration of PCS arrhythmia; denervation of the heart reduced the duration of PCS arrhythmia. Ouabain (0.05 mg/kg iv) reduced the duration of PCS arrhythmia in dogs with denervated hearts. These findings indicate that PCS arrhythmia in dogs is norepinephrine dependent. Evidence indicated that ouabain has an antiadrenergic action on the heart also is presented.From the Studies on the physiology of countershock, in preparation. LEAD I FROM DOGA -I5v Trigger input B -Sawtooth output C " Sowtooth input D " Pulse output E -Gate output ELECTRONICS FOR MEDICINE FIGURE 1A block diagram of the electronic circuitry used. This apparatus can be assembled from standard eQuipment which is available in most laboratories. A is the "trigger in" (15 v) of a Tektronix waoeform generator (WFC) operated in the "triggered" mode. The triggering pulse is a 4 msec, 15 v, square wave supplied by the Schmitt trigger. B is the "sawtooth out"; C is the "sawtooth input" of a pulse generator (PC); D is the "pulse output" of a pulse generator; and E is the "gate output" of a pulse generator.

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Effect of Quinidine and Pronethalol on Acetylstrophanthidin-Induced Ventricular Arrhythmia in Cats Treated with Reserpine

Cited by 24 publications

References 16 publications

Influence of Pronethalol on Ouabain Toxicity in Dogs Treated with Reserpine

Influence of Pronethalol on Ouabain Toxicity in Dogs Treated with Reserpine

Effect of Various Antiarrhythmic Drugs on the Daunomycin-Induced Arrhythmia in the Hamster

Post-Countershock Arrhythmias in Untreated and Digitalized Dogs

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