Effects of various hypoglycaemic sulphonylureas on the cardiotoxicity of glycosides

Pogátsa, G; Koltai, M; I, Balkányi; Devai, J.; Kiss, V.

doi:10.1007/bf00544351

Cited by 16 publications

(14 citation statements)

References 14 publications

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“…This drug can attenuate the ischemically induced changes in the ST-segment in intact anesthetized or unanesthetized animals [Kondo et al, 1996;Billman et al, 1998]. Glibenclamide also prevented arrhythmias induced by ischemia in isolated hearts [Pogatsa et al, 1988;Wolleben et al, 1989;Kantor et al, 1990;Gwilt et al, 1992;Tosaki et al, 1995]. Furthermore, both glibenclamide and glimepride reduced blood glucose and decreased the incidence of irreversible ventricular fibrillation induced by reperfusion (after a 6-minute coronary occlusion) in anesthetized rats [El Reyani et al, 1999].…”

Section: Atp-sensitive Potassium Channel Antagonists: Ischemia-selectmentioning

confidence: 99%

Animal models of lethal arrhythmias

Billman

2002

Drug Development Research

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Sudden cardiac death resulting from ventricular tachyarrhythmias remains the leading cause of death in industrially developed countries, accounting for between 300,000 and 500,000 deaths each year in the United States. Yet, despite the enormity of this problem, the development of safe and effective antiarrhythmic agents remains elusive. Indeed, several class I (encainide and flecainide) and class III (dsotalol) drugs have actually been shown to increase, rather than decrease, the risk of arrhythmic death in patients recovering from myocardial infarction. The identification of effective antiarrhythmic agents is critically dependent on the use of appropriate animal models of human disease. In particular, myocardial ischemia may be an important determinant for the development of the life-threatening ventricular arrhythmias. For example, preclinical studies demonstrate that many drugs that prevent arrhythmias induced by programmed electrical stimulation fail to prevent ventricular fibrillation provoked by ischemia in the same animals. Thus, one would predict that animal models in which lethal arrhythmias are induced by myocardial ischemia would be the most effective tools for the identification of potential antiarrhythmic medications. This review first evaluates several animal models of lethal ventricular arrhythmias with particular emphasis placed on canine models. Then it closes with a brief discussion of ATP-sensitive potassium-channel antagonists as an example of antiarrhythmic drugs that may act selectively on the ischemic myocardium. Drug Dev. Res. 55:59-72, 2002.

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Section: Atp-sensitive Potassium Channel Antagonists: Ischemia-selectmentioning

confidence: 99%

Animal models of lethal arrhythmias

Billman

2002

Drug Development Research

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“…It has been reported, in rabbits and rats, that glibenclamide decreased, but tolbutamide and carbutamide increased strophanthidin toxicity (Pogatsa, Koltai, Balkanyi, Devai & Kiss, 1985; Pogatsa et al. , 1988).…”

Section: Katp Channels and Potassium Currentsmentioning

confidence: 99%

“…Concomitantly administered diuretic agents may increase the incidence of digitalis toxicity both by decreasing the glomerular filtration rate caused by volume depletion and by inducing a variety of electrolyte disturbances, including hypokalaemia, hypomagnesaemia, and (for thiazide diuretics) hypercalcaemia (Hauptman & Kelly, 1999;Ma, Brady, Pollack & Chan, 2001). It has been reported that in digitalized non‐insulin‐dependent diabetics, multifocal ectopic ventricular beats could be observed in none among the 80 glibenclamide‐treated diabetics (Pogatsa et al. , 1988).…”

Section: Clinical Studiesmentioning

confidence: 99%

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Cardiotoxicity of digitalis glycosides: roles of autonomic pathways, autacoids and ion channels

Demiryürek

2005

Auton Autocoid Pharmacol

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1 Cardiac glycosides have been used for centuries as therapeutic agents for the treatment of heart diseases. In patients with heart failure, digoxin and the other glycosides exert their positive inotropic effect by inhibiting Na(+)-K(+)-ATPase, thereby increasing intracellular sodium, which, in turn, inhibits the Na(+)/Ca(2+) exchanger and increases intracellular calcium levels. As the therapeutic index of digitalis is narrow, arrhythmias are common problems in clinical practice. The mechanisms and mediators of these arrhythmias, however, are not completely understood. 2 The involvement of the sympathetic and parasympathetic nervous system in digitalis cardiac toxicity is reviewed. 3 Receptors, channels, exchange systems or other cellular components involved in digitalis-induced cardiotoxicity are also reviewed. 4 Possible mediators of digitalis-induced cardiac toxicity are discussed. 5 Management of digitalis toxicity in patients is summarized. 6 The determination of the possible mediators of digitalis-induced cardiac toxicity will enhance our knowledge and lead to the development of new therapeutic strategies to treat these lethal arrhythmias.

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“…22 In addition, drug interactions can cause profound hypoglycemia (Table 2). [23][24][25][26][27][28][29][30][31][32][33] Factors that increase the risk of having a hypoglycemic episode include advanced age, poor nutrition, alcohol consumption, renal and hepatic disease, and polypharmacy. 2,34 Clinically, time to peak and duration of action are the most important considerations when anticipating hypoglycemia after sulfonylurea overdose (Table 1).…”

Section: S U L F O N Y L U R E a Smentioning

confidence: 99%