The effects of bisaramil on experimental arrhythmias

Paróczai, M; Kárpáti, E; Solti, F

doi:10.1016/1043-6618(90)90753-z

Cited by 17 publications

(6 citation statements)

References 11 publications

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“…The currents evoked are shown plotted at the time that they were evoked, normalized to the size of the first current. The dotted line shows the fit of the equation l-[P.(o/eC/Ti) + ((l m)/eC/I2)] to the peak current amplitude with 13=0.65, a = 0.6, T1 = 40 ms and T2 = 5 s. bisaramil probably produces its anti-arrhythmic actions via blockade of cardiac sodium channels (Paroczai et al, 1990;Haruno & Hashimoto, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…This spectrum of actions is very similar to that seen with class I anti-arrhythmic agents, eg. lignocaine (Bean et al, 1983) and quinidine (Snyders & Hondeghem, 1990 bisaramil probably produces its anti-arrhythmic actions via blockade of cardiac sodium channels (Paroczai et al, 1990;Haruno & Hashimoto, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown to be effective against both chemical and ischaemic models of arrhythmogenesis (Paroczai et al, 1990;Haruno & Hashimoto, 1993). In isolated cardiac tissue, bisaramil produces an increase in ventricular fibrillation thresholds (Paroczai et al, 1990). In addition it decreases V,.,,, action potential amplitude and overshoot potentials in guinea-pig papillary muscle (Sunami et al, 1991;Paroczai et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Tonic and use‐dependent block of sodium currents in isolated cardiac myocytes by bisaramil

Saint

1995

British J Pharmacology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Tonic and use‐dependent block of sodium currents in isolated cardiac myocytes by bisaramil

Saint

1995

British J Pharmacology

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“…The utility of aconitine for the study of electrocardiographic activity is well documented. This drug has been used experimentally in anesthetized rats to investigate the vulnerability to ventricular arrhythmias as well as the efficacy of antiarrhythmic drugs (2,18,30,40).…”

mentioning

confidence: 99%

Increased susceptibility to ventricular arrhythmias in a rodent model of experimental depression

Grippo¹,

Santos²,

Johnson³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Depression is an important public health problem and is considered to be an independent risk factor for coronary artery disease. The pathophysiological mechanisms that link depression with adverse cardiovascular events (e.g., myocardial ischemia, myocardial infarction, and sudden death) are not well established. It is possible that an increased susceptibility to life-threatening cardiac arrhythmias in depressed patients influences the risk of morbidity and mortality in coronary artery disease. This idea was tested with the use of an experimental model of depression that was developed to induce anhedonia, the reduced responsiveness to pleasurable stimuli observed in human depressed patients. Rats exposed to 4 wk of chronic mild stress (e.g., paired housing, strobe light, and white noise) displayed anhedonia, which was operationally defined by the reduced intake of a palatable sucrose solution relative to an established baseline and to control animals. Furthermore, compared with control rats, the anhedonic rats showed increased basal heart rate and decreased heart rate variability. In response to an intravenously infused chemical challenge, aconitine, anhedonic rats exhibited an increased vulnerability to ventricular arrhythmias, as indicated by a reduced threshold for premature ventricular complexes, salvos, and ventricular tachycardia. These findings suggest that the presence of depressive symptoms is associated with a lower threshold for ventricular arrhythmias, which may contribute to the increased risk for adverse cardiovascular events in patients with depression.

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Synthesis of Natural Compounds Based on the [3,7]‐Diazabicyclo[3.3.1]nonane (Bispidine) Core

Sacchetti

Rossetti

2021

Eur J Org Chem

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The [3,7]‐diazabicyclo[3.3.1]nonane (bispidine) structure is found in several interesting naturally occurring alkaloids. The most representative components are the tetracyclic alkaloid (−)‐sparteine and the tricyclic (−)‐cytisine alkaloids. Their biological activities have been known for a long time. In the literature, different syntheses of both tetracyclic and tricyclic structures have been reported, especially in the last few years, when a number of new reports renewed the interest in these fascinating molecules. Bicyclic bispidine derivatives have been thoroughly investigated in recent times also for their applications as catalysts, metal chelating agents, and lately in coordination polymers chemistry. In this review, we describe the most relevant strategies for the synthesis of molecules based on the [3,7]‐diazabicyclo[3.3.1]nonane core, related to (−)‐sparteine and (−)‐cytisine alkaloids.

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The effects of bisaramil on experimental arrhythmias

Cited by 17 publications

References 11 publications

Tonic and use‐dependent block of sodium currents in isolated cardiac myocytes by bisaramil

Tonic and use‐dependent block of sodium currents in isolated cardiac myocytes by bisaramil

Increased susceptibility to ventricular arrhythmias in a rodent model of experimental depression

Synthesis of Natural Compounds Based on the [3,7]‐Diazabicyclo[3.3.1]nonane (Bispidine) Core

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