Effects of glibenclamide, metformin and insulin on the incidence and latency of death by oubain-induced arrhythmias in mice

Yazar, Aziz; Polat, Gürbüz; Ün, İsmail; Levent, Adnan; Kaygusuz, Ayşe; Büyükafşar, Kansu; Ankaralı, Handan

doi:10.1006/phrs.2001.0944

Cited by 9 publications

(7 citation statements)

References 18 publications

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“…106 These results are consistent with another observation that the acute metformin treatment affected neither the incubation period nor the mortality rate. 107 Gap junction channels are necessary for propagating the action potential among adjacent cardiomyocytes. 108 Abnormal expression of connexin 43 (Cx43) causes gap junction remodelling and cardiac arrhythmias.…”

Section: Ampk-related Actions Of Metformin In Arrhythmiamentioning

confidence: 99%

Protective effects of metformin in various cardiovascular diseases: Clinical evidence and AMPK‐dependent mechanisms

Peng

Tang

et al. 2022

J Cellular Molecular Medi

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Metformin, a well‐known AMPK agonist, has been widely used as the first‐line drug for treating type 2 diabetes. There had been a significant concern regarding the use of metformin in people with cardiovascular diseases (CVDs) due to its potential lactic acidosis side effect. Currently growing clinical and preclinical evidence indicates that metformin can lower the incidence of cardiovascular events in diabetic patients or even non‐diabetic patients beyond its hypoglycaemic effects. The underlying mechanisms of cardiovascular benefits of metformin largely involve the cellular energy sensor, AMPK, of which activation corrects endothelial dysfunction, reduces oxidative stress and improves inflammatory response. In this minireview, we summarized the clinical evidence of metformin benefits in several widely studied cardiovascular diseases, such as atherosclerosis, ischaemic/reperfusion injury and arrhythmia, both in patients with or without diabetes. Meanwhile, we highlighted the potential AMPK‐dependent mechanisms in in vitro and/or in vivo models.

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Section: Ampk-related Actions Of Metformin In Arrhythmiamentioning

confidence: 99%

Protective effects of metformin in various cardiovascular diseases: Clinical evidence and AMPK‐dependent mechanisms

Peng

Tang

et al. 2022

J Cellular Molecular Medi

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“…Moreover, diabetic+Glibenclamide mice received Glibenclamid 1 mg/kg I.P as a treatment. 20,21 Non-diabetic hyperglycemia Acute hyperglycemia was induced by I.P injection of dextrose (2 g/kg body weight) 30 min prior to PTZ injection and seizure induction.…”

Section: Stz-induced Diabetesmentioning

confidence: 99%

Pentylenetetrazol-induced seizures strength in diabetic and normal serum glucose elevated male mice

2016

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Background: Epilepsy is one of the most important neurological disorders, afflicting both genders during their lifetime. Metabolic disturbances, including hyperglycemia and hypoglycemia, are one of the main reasons of seizures in which frequently have been seen in diabetes mellitus. A large body of literature has investigated correlation between hyperglycemia, hypoglycemia and seizure. However, a definitive conclusion has not been taken, yet. Hence, we developed a rodent model of PTZ-induced seizure in order to investigate about relation between PTZ-induced seizures and glycemic changes, including diabetic and non-diabetic hyperglycemia and hypoglycemia.Methods: We chose 50 naive, adult male inbred mice of the Balb/c strain (aged 8–10 weeks, weighted 25-35 grams) and divided them into 5 groups, randomly (n=10 in each groups): 1. Control (received saline and citrate buffer). 2. Diabetic group (received STZ 140 mg/kg I.P). 3. Diabetic+Glibenclamide group (received STZ 140 mg/kg I.P and treated with Glibenclamide 1 mg/kg I.P daily). 4. Non-diabetic hyperglycemic group (received glucose "D-dextrose" 2 g/kg I.P 30 min before PTZ administration. 5. Hypoglycemic group (the animals were fasted one day other days during experimental period). Chemical kindling was induced by PTZ injection (35 mg/kg, I.P), every other days (11 periods that lasted 22 days). Results: Our data shown non-diabetic hyperglycemic mice that had elevated blood glucose levels, were more resistant to seizures compared to control group (p<0.05). Threshold and duration of the second phase of the seizures in non-diabetic hyperglycemic mice were increased (p<0.001). Moreover, threshold of the phase 5 was enhanced (p<0.001). Again, hypoglycemic mice had statistically significant decrease in threshold of phase 5 compared to control group (p<0.05).Conclusions: We found that acute non-diabetic hyperglycemia not only have had no aggravating effects on seizure susceptibility but also have shown anticonvulsive effects. As well, we found that hypoglycemia has decreased threshold of phase 5 in challenge dose, i.e. onset of the most severe phase of the seizures was accelerated.

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“…Inhibition of K ATP channels by sulphonylureas decreased strophanthin cardiotoxicity in rabbits (Pogatsa, 1995). Glibenclamide at low doses can be an effective antiarrhythmic agent against ouabain‐induced arrhythmias in mouse (Yazar et al. , 2002).…”

Section: Katp Channels and Potassium Currentsmentioning

confidence: 99%

“…Insulin has been reported to stimulate ionic transport by the sodium pump and induce hyperpolarization in skeletal and cardiac muscle among other cells (Ruiz‐Ceretti, DeLorenzi, Lafond & Chartier, 1988). Insulin, at low doses, can be an effective antiarrhythmic agent against ouabain‐induced arrhythmias in mice (Yazar et al. , 2002).…”

Section: Katp Channels and Potassium Currentsmentioning

confidence: 99%

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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Effects of glibenclamide, metformin and insulin on the incidence and latency of death by oubain-induced arrhythmias in mice

Cited by 9 publications

References 18 publications

Protective effects of metformin in various cardiovascular diseases: Clinical evidence and AMPK‐dependent mechanisms

Protective effects of metformin in various cardiovascular diseases: Clinical evidence and AMPK‐dependent mechanisms

Pentylenetetrazol-induced seizures strength in diabetic and normal serum glucose elevated male mice

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

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