Some Factors Affecting Ouabain‐induced Ventricular Arrhythmia in the Reserpine‐treated Cat*

Ciofalo, Frank R.; Levitt, Barrie; Roberts, Jay

doi:10.1111/j.1476-5381.1967.tb02120.x

Cited by 12 publications

(4 citation statements)

References 11 publications

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“…In a suibsequent paper Cairoli, Reilly, Ito & Roberts (1962) reported that reserpine pretreatment in dogs significantly increased the amount of acetyl-strophanthidin required to produce ventricular arrhythmias. Ciofalo, Levitt & Roberts (1967) found that the onset of arrhythmias induced by ouaibain in cats was delayed by pretreatment with reserpine. Finally, Barrett & Cullum (1968) showed that (-)-propranolol was more effective than (+)-propranolol in reversing ouabain-induced ventricular tachycardia in dogs.…”

Section: Discussionmentioning

confidence: 97%

The relevance of β‐receptor blockade to ouabain‐induced cardiac arrhythmias

Dohadwalla

Freedberg

Williams

1969

British J Pharmacology

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. (+)‐propranolol and (±)‐propranolol are comparable in their potency as a local anaesthetic on the intact and desheathed frog sciatic nerve. . (±)‐propranolol is much more potent than (+)‐propranolol as a β‐receptor blocking agent and also more effective than the latter in protecting guinea‐pigs against ouabain‐induced ventricular fibrillation. . In isolated rabbit atria (–)‐, (+)‐ and (±)‐propranolol, and I.C.I. 50172, which has hardly any local anaesthetic activity, greatly reduce the rate of rise of the intracellularly recorded action potential at concentrations which have no significant effect on electrical threshold, contractions, spontaneous frequency, maximum driving frequency, repolarization time or conduction velocity.

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Section: Discussionmentioning

confidence: 97%

The relevance of β‐receptor blockade to ouabain‐induced cardiac arrhythmias

Dohadwalla

Freedberg

Williams

1969

British J Pharmacology

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“…Data for the con trol ouabain group (12 cats) and the II cats pretreated with timolol (5 mg/kg, i.v.) 25 min prior to ouabain, were previously reported by Lathers [5], Similar doses to arrhythmia and death have also been reported in other studies [2,6,7], Arrhythmia was defined as the first occurrence (intermittent or sustained) of the loss of normal sinus rhythm due to the disappearance of the P wave or to the appearance of ventricular complexes. Sinus bra dycardia or tachycardia were not defined as arrhyth mia.…”

Section: Methodsmentioning

confidence: 78%

“…The administration of intravenous oua bain provides a reproducible model of car diac arrhythmias and has been extensively used for this purpose [2][3][4][5][6][7]. An increase in the dose of ouabain which produces the de velopment of arrhythmia and death demon strates an antiarrhythmic effect of a drug.…”

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confidence: 99%

Protection of CGS 10078B against Ouabain-Induced Arrhythmia in the Cat

Lathers¹,

Tümer²,

Frame³

et al. 1987

Pharmacology

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CGS 10078B (CGS; l-[2,3-dihydro-l,4-(2S)-benzodioxm-2-yl]-5-[2,3-dihydro-1,4-(2i?)-benzodioxin-2-yl]-3-(1R,55)-aza-1,5-pentanediol methane sulfonate) is an agent with α- and β-receptor and calcium channel blocking actions. To study its antiarrhythmic activity, cats were anesthetized with α-chloralose, ventilated, and given atropine and gallamine. CGS (10 or 20 mg/kg, i.v.) was infused 15 min prior to ouabain. Bolus injections of ouabain (25 μg/kg, i.v.) were given every 15 min until death (D). Some cats were pretreated with reserpine (R; 5 mg/kg, i.p.) 24 h prior to the experiment. In other cats 6-hydroxydopamine (6-OHDA; 20 mg/kg, i.v.) was administered 3 days prior to CGS 20 mg/kg and ouabain. Data were compared with those of Lathers [Eur. J. Pharmacol. 64: 95, 1980], i.e., with 12 cats who received only ouabain and with 11 pretreated with timolol (T; 5 mg/kg, i.v.) prior to ouabain. After CGS (10 or 20 mg/kg, i.v.), but just prior to the first dose of ouabain, the blood pressure (BP) was decreased (p < 0.05) from control (165 ± 6 vs. 96 ± 7, and 136 ± 5 vs. 90 ± 10 mm Hg, respectively). Comparable heart rate (HR) values were also decreased (p < 0.05) from 225 ± 17 to 166 ± 14 and from 193 ± 8 to 152 ± 6beats/min. 11 min after T, BP and HR had decreased (p < 0.05) from 133 ± 6 to 103 ± 7 mm Hg and from 134 ± 4 to 104 ± 6 beats/min, respectively. Ouabain did not influence these decreases in BP and HR. CGS (10 or 20 mg/kg, i.v.) increased (p < 0.05) the time to ouabain-induced arrhythmia (AR) and D. The magnitude of the protection appeared to be similar to that afforded by T. R given prior to CGS (20 mg/kg, i.v.) also increased the time to ouabain-induced AR and D while 6-OHDA increased the time to AR. The CGS protection against ouabain-induced AR was still present in animals pretreated with R or 6-OHDA. This indicates that the antiarrhythmic affect is not dependent upon adrenergic neuronal blockade.

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“…In fact, diis substance did not change significantly die blood pressure as compared to the control, eitiier when given intraventricularly or intravenously. However, different procedures, which were shown to confer protection, also give rise to a marked hypotension (4).…”

Section: Discussionmentioning

confidence: 99%

Modification of the Cardiotoxic Effects of Ouabain by Acepromazine, Tetrodotoxin and Magnesium Sulphate

Peres-Gomes

Ribeiro

1979

Pharmacology

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Acepromazine (500 μg), tetrodotoxin (0.5 μg) and magnesium sulphate (7.5 mg twice) given intracerebroventricularly increased the doses of ouabain given by continuous intravenous infusion, required to induce arrhythmias and death. Acepromazine (150 μg kg^–1) was also effective when administered intravenously. Acepromazine (1.5 mg kg^–1) and tetrodotoxin (4-6μg kg^–1) given intravenously did not protect against, and even increased, the toxicity of ouabain. Both substances decreased blood pressure and increased heart rate. Tetrodotoxin, but neither acepromazine nor magnesium sulphate given intracerebroventricularly, induced a decrease in the heart rate before ouabain infusion. Acepromazine (500 μg) and tetrodotoxin (0.5 μg), but not magnesium sulphate, given intracerebroventricularly, decreased the blood pressure before ouabain infusion. The results are discussed in relation to the effects of those substances and ouabain on the circulation, and to the fact that the cardiac arrhythmias induced by high doses of ouabain and the protection obtained with tetrodotoxin and magnesium sulphate are, at least in part, mediated by the central nervous system.

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Some Factors Affecting Ouabain‐induced Ventricular Arrhythmia in the Reserpine‐treated Cat*

Cited by 12 publications

References 11 publications

The relevance of β‐receptor blockade to ouabain‐induced cardiac arrhythmias

The relevance of β‐receptor blockade to ouabain‐induced cardiac arrhythmias

Protection of CGS 10078B against Ouabain-Induced Arrhythmia in the Cat

Modification of the Cardiotoxic Effects of Ouabain by Acepromazine, Tetrodotoxin and Magnesium Sulphate

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