Antiarrhythmic Compounds

Szekeres, L.; Papp, Julius Gy.

doi:10.1007/978-3-0348-7065-8_5

Cited by 11 publications

(16 citation statements)

References 166 publications

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“…Doses of guanethidine required to render the atrial membrane inexcitable are probably too high to be involved in the mechanism of the antiarrhythmic action. The adrenergic neurone blocking action may be a specific and major factor for the antiarrhythmic properties (Szekeres & Papp, 1968;Roberts, Kelliher & Lathers, 1976).…”

Section: Effects Ofpretreatment With a Low Dose Of Tetrodotoxin On Gumentioning

confidence: 99%

Action of Guanethidine on Rabbit Atrial Membranes

Misu

Nishio

1978

British J Pharmacology

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Intracellular potentials were recorded in driven left atria from reserpine‐treated rabbits. Guanethidine 2 × 10−5m slightly increased Vmax and shortened the total duration (TD) of the action potential (AP) without causing hyperpolarization. For the first 30 min after 4 × 10−4m, Vmax increased without hyperpolarization and AP height increased slightly. Thereafter, Vmax and height decreased with a slight and gradual depolarization. This depolarization was irreversible. TD was increased after 15 minutes. Guanethidine 2 × 10−3 M initially decreased Vmax and height before causing depolarization. Pretreatment with tetrodotoxin (TTX) 1.6 × 10−7m prevented or reversed the initial increases in Vmax, height and TD induced by guanethidine (4 × 10 −4m). TTX 3.1 to 6.2 × 10−6m, added 15 or 30 min after guanethidine 4 × 10−4m, delayed or prevented depolarization by guanethidine. Ouabain 10−5m incubated for 20 and 90 min greatly inhibited Na+, K+‐adenosine triphosphatase and K+‐phosphatase activities; guanethidine was without effect. Guanethidine probably increases resting sodium permeability after the promotion of increases in sodium permeability during the AP. High doses of the drug decrease sodium permeability during the AP.

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Section: Effects Ofpretreatment With a Low Dose Of Tetrodotoxin On Gumentioning

confidence: 99%

Action of Guanethidine on Rabbit Atrial Membranes

Misu

Nishio

1978

British J Pharmacology

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“…Since the mechanisms involved in the production of cardiac arrhythmias are not clear ly understood (13,14) and since no single animal technique is adequate in investigating the antiarrhythmic activity of a drug (15), a variety of test-procedures have been employed in the present study in order to make an assessment of the spectrum of antiarrhythmic activity of piperacetazine and benzosulfonate. It has been found that both the drugs are effective in causing a significant reduction in the duration of acetylcholine-induced atrial fibrillation, in establishing the end-point in aconitine-induced atrial arrhythmia and in reverting the injury-cum-stimulation-induced atrial flutter to normal sinus rhythm.…”

Section: Discussionmentioning

confidence: 99%

Effect of Two Recently Synthesized Phenothiazine Derivatives Upon Experimental Cardiac Arrhythmias

Madan

1971

Jpn.J.Pharmacol

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Chlorpromazine has been reported to suppress cardiac arrhythrnias produced ex perimentally (1, 2) and those observed in clinical practice (3). Two new phenothiazine derivatives, namely piperacetazine (2-acetyl-10-{-3 [-4-(fl-hydroxyethyl)-piper] dine] pro pyl}-phenothiazine) and benzosulfonate (1-methyl-2-{-(2-methylsulfinyl-dibenzothiazinyl 10)-ethyl-1 }-piperidine) have been recently synthesized (4, 5). Hence it is of interest to determine if they possess antiarrhythmic activity. MATERIAL AND METHODSFreshly prepared I % solutions in isotonic saline of benzosulfonate and piperacetazine were used. Cardiac arrhythmias were produced in vagotornized mongrel dogs of both sexes weighing between 8 and 18 kg by the following techniques:1. Acetylcholine-induced atrial fibrillation Twelve animals were anaesthetized with intravenous pentobarbital sodium, 30 mg/ kg. Atrial fibrillation was produced according to the method of Scherf and Chick (6) which was followed in all essential details as described by Schallek (7). A small pledget of cotton soaked in 5 per cent acetylcholine was placed on the area of sino-atrial node.One minute later, atrial fibrillation was induced by pinching the atrium and its duration noted. Two such controls were taken after which the procedure was repeated a third time. After the atria were fibrillating for a minute, the drug to be tested was injected and reduction in the duration of fibrillation noted. Atrial flutter incluced by injury-stimulationAccording to the method of Rosenblueth and Garcia Ramos (8) 3. Aconitine-induced atrial arrhythmia Atrial arrhythmia was produced by the method of Scherf (9) in 13 dogs which were anaesthetized as above. A cotton pledget soaked in 0.05% solution of aconitine hydro

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“…Quinidine (I) is the prototype of this class of agents; consequently, agents exhibiting this type of antiarrhythmic action are said to possess "quinidine-like" properties (16).…”

Section: Mechanism Of Action Of Antiarrhythmic Drugsmentioning

confidence: 99%

“…Since the development of the technique for recording the transmembrane action potential of cardiac cells, many studies have elucidated the effects of antiarrhythmic drugs on these parameters. Numerous reviews of the subject have appeared (15)(16)(17)23,61,65,(69)(70)(71)(72)(73)(74)76,89,94,(136)(137)(138)(139)(140)(141)(142).…”

Section: Mechanism Of Action Of Antiarrhythmic Drugsmentioning

confidence: 99%