Electrocardiological effects of ranolazine and lidocaine on normal and diabetic rat atrium.


Journal

Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing
ISSN: 1572-8595
Titre abrégé: J Interv Card Electrophysiol
Pays: Netherlands
ID NLM: 9708966

Informations de publication

Date de publication:
Apr 2021
Historique:
received: 06 01 2020
accepted: 30 03 2020
pubmed: 25 4 2020
medline: 19 8 2021
entrez: 25 4 2020
Statut: ppublish

Résumé

Cellular changes occurring in diabetic cardiomyopathy include disturbances of calcium and sodium homeostasis. Voltage-gated sodium channels are responsible for the initiation of cardiac action potentials, and the excitability would create relevance. The effect of ranolazine as a sodium channel blocker on atrium electromechanical parameters is investigated and compared with lidocaine in streptozocin-treated diabetic rats. After an 8-week induction of diabetes type I, the effect of cumulative concentrations of ranolazine and lidocaine on the electrophysiology of isolated atrium was studied. Ranolazine's effects were evaluated on cardiac sodium current in normal- and high-glucose medium, with whole-cell patch-clamp technique. Ranolazine at therapeutic concentrations had no significant statistical effect on refractory period in normal and diabetic isolated heart. Ranolazine (10 μM) caused a hyperpolarizing shift of V It is concluded that in the isolated rat atrium preparation, ranolazine and lidocaine have no beneficial on diabetic cardiomyopathy. Although refractoriness and contractility were not much different in normal and diabetic atria, there was a definite effect of ranolazine and lidocaine on sodium current in varying concentrations. This may have significance in future therapeutics.

Identifiants

pubmed: 32328860
doi: 10.1007/s10840-020-00742-w
pii: 10.1007/s10840-020-00742-w
doi:

Substances chimiques

Acetanilides 0
Piperazines 0
Sodium Channel Blockers 0
Lidocaine 98PI200987
Ranolazine A6IEZ5M406

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

387-394

Subventions

Organisme : Shiraz University of Medical Sciences
ID : 89-5404

Références

Dobrev D, Nattel S. New antiarrhythmic drugs for treatment of atrial fibrillation. Lancet. 2010;375:1212–23.
doi: 10.1016/S0140-6736(10)60096-7
Undrovinas NA, Maltsev VA, Belardinelli L, Sabbah HN, Undrovinas A. Late sodium current contributes to diastolic cell ca2+ accumulation in chronic heart failure. J Physiol Sci. 2010;60:245–57.
doi: 10.1007/s12576-010-0092-0
Burashnikov A, Antzelevitch C. Atrial-selective sodium channel blockers: do they exist? J Cardiovasc Pharmacol. 2008;52:121–8.
doi: 10.1097/FJC.0b013e31817618eb
Sossalla S, Maier LS. Role of ranolazine in angina, heart failure, arrhythmias, and diabetes. Pharmacol Ther. 2012;133:311–23.
doi: 10.1016/j.pharmthera.2011.11.003
Casis O, Gallego M, Iriarte M, Sanchez-Chapula JA. Effects of diabetic cardiomyopathy on regional electrophysiologic characteristics of rat ventricle. Diabetologia. 2000;43:101–9.
doi: 10.1007/s001250050013
Bilginoglu A, Kandilci HB, Turan B. Intracellular levels of Na(+) and TTX-sensitive Na(+) channel current in diabetic rat ventricular cardiomyocytes. Cardiovasc Toxicol. 2013;13:138–47.
doi: 10.1007/s12012-012-9192-9
Soliman D, Wang L, Hamming KSC, Yang W, Fatehi M, Carter CC, et al. Late sodium current inhibition alone with ranolazine is sufficient to reduce ischemia- and cardiac glycoside-induced calcium overload and contractile dysfunction mediated by reverse-mode sodium/calcium exchange. J Pharmacol Exp Ther. 2012;343:325–32.
doi: 10.1124/jpet.112.196949
Luan R, Liu S, Yin T, Lau WB, Wang Q, Guo W, et al. High glucose sensitizes adult cardiomyocytes to ischaemia/reperfusion injury through nitrative thioredoxin inactivation. Cardiovasc Res. 2009;83:294–302.
doi: 10.1093/cvr/cvp085
D’Amico M, Marfella R, Nappo F, Di Filippo C, De Angelis L, Berrino L, et al. High glucose induces ventricular instability and increases vasomotor tone in rats. Diabetologia. 2001;44:464.
doi: 10.1007/s001250051644
Bich-Hoai TT, Marin A, Dinu C, Banciu D, Maria-Luiza F, Ristoiu V. Hypoxia and high glucose activate tetrodotoxin-resistant Na+ currents through PKA and PKC. Acta Neurobiol Exp. 2010;70:351–61.
Rajamani S, El-Bizri N, Shryock JC, Makielski JC, Belardinelli L. Use-dependent block of cardiac late Na+ current by Ranolazine. Heart Rhythm. 2009;6:1625–31.
doi: 10.1016/j.hrthm.2009.07.042
El-Menyar AA. Dysrhythmia and electrocardiographic changes in diabetes mellitus: pathophysiology and impact on the incidence of sudden cardiac death. J Cardiovasc Med. 2006;7:580–5.
doi: 10.2459/01.JCM.0000237904.95882.c8
Warley A. Changes in sodium concentration in cardiac myocytes from diabetic rats. Scanning Microsc. 1991;5:239–44 discussion 244-5.
pubmed: 1828909
Katoh H, Noda N, Hayashi H, Satoh H, Terada H, Ohno R, et al. Intracellular sodium concentration in diabetic rat ventricular myocytes. Jpn Heart J. 1995;36:647–56.
doi: 10.1536/ihj.36.647
Pierce GN, Ramjiawan B, Dhalla NS, Ferrari R. Na(+)-H+ exchange in cardiac sarcolemmal vesicles isolated from diabetic rats. Am J Phys. 1990;258(1 Pt 2):H255–61.
Otake H, Suzuki H, Honda T, Maruyama Y. Influences of autonomic nervous system on atrial arrhythmogenic substrates and the incidence of atrial fibrillation in diabetic heart. Int Heart J. 2009;50:627–41.
doi: 10.1536/ihj.50.627
Watanabe M, Yokoshiki H, Mitsuyama H, Mizukami K, Ono T, Tsutsui H. Conduction and refractory disorders in the diabetic atrium. Am J Physiol Heart CircPhysiol. 2012;303:H86–95.
doi: 10.1152/ajpheart.00010.2012
Savabi F, Kirsch A. Altered functional activity and anoxic tolerance in diabetic rat isolated atria. Arch Biochem Biophys. 1990;279:183–7.
doi: 10.1016/0003-9861(90)90479-I
Stables CL, Musa H, Mitra A, Bhushal S, Deo M, Guerrero-Serna G, et al. Reduced Na
doi: 10.1016/j.yjmcc.2013.12.031
Bracken NK, Woodall AJ, Howarth FC, Singh J. Voltage-dependence of contraction in streptozotocin-induced diabetic myocytes. Mol Cell Biochem. 2004;261:235–43.
doi: 10.1023/B:MCBI.0000028761.61216.5e
Khazraei H, Mirkhani H, Purkhosrow A. Vasorelaxant effect of ranolazine on isolated normal and diabetic rat aorta: a study of possible mechanisms. Acta Physiol Hung. 2013;100:153–62.
doi: 10.1556/APhysiol.100.2013.2.3
Khazraei H, Shafa M, Mirkhani H. Effect of ranolazine on cardiac microcirculation in normal and diabetic rats. Acta Physiol Hung. 2014;101:301–8.
doi: 10.1556/APhysiol.101.2014.3.5
Khazraei H, Mirkhani H, Akmali M. The antianginal agent ranolazine inhibits mitochondrial β-oxidation pathway. Clin Exp Pharmacol. 2016;6:2.
Choi KM, Zhong Y, Hoit BD, Grupp IL, Hahn H, Dilly KW, et al. Defective intracellular Ca+2 signalling contribute to cardiomyopathy in type I diabetic rats. Am J Physiol Heart Circ Physiol. 2002;283:H1398–408.
doi: 10.1152/ajpheart.00313.2002
Dillmann WH. Overexpression of sarcoplasmic reticulum Ca+2-ATPase improves myocardial contractility in diabetic cardiomyopathy. Diabetes. 2002;51:1166–71.
doi: 10.2337/diabetes.51.4.1166
Howarth FC, Jacobson M, Qureshi MA. Altered gene expression may underlie prolonged duration of the QT interval and ventricular action potential in streptozotocin-induced diabetic rat heart. Mol Cell Biochem. 2009;328:57–65.
doi: 10.1007/s11010-009-0074-9

Auteurs

Hajar Khazraei (H)

Colorectal research center, Shiraz University of Medical Sciences, Shiraz, Iran.

Hossein Mirkhani (H)

Department of pharmacology, Shiraz University of Medical Sciences, Shiraz, Iran. khazraee@sums.ac.ir.

Waheed Shabbir (W)

Department of Pharmacology and Toxicology, University of Vienna, A-1090, Vienna, Austria.

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