Volume 15, Issue 2 (Summer 2011)                   Physiol Pharmacol 2011, 15(2): 249-259 | Back to browse issues page

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Khori V, Shariatnejad S, Alizadeh A, Yazdi H, Pourabouk M, Badaghabadi F, et al . Protective role of cyclosporine on the model simulated the rotational nodal arrhythmia (AVNRT) by using extracellular field potential recordings of isolated atrioventricular-node of rabbit. Physiol Pharmacol 2011; 15 (2) :249-259
URL: http://ppj.phypha.ir/article-1-703-en.html
Protective role of cyclosporine on the model simulated the rotational nodal arrhythmia (AVNRT) by using extracellular field potential recordings of isolated atrioventricular-node of rabbit
Vahid Khori , Sepideh Shariatnejad , Alimohammad Alizadeh , Hamidreza Yazdi , Mona Pourabouk , Fakhri Badaghabadi , Hamid Reza Moheimani , Shima Changizi , Maryam Rajee , Mohsen Nayebpour
Abstract:   (11942 Views)
Introduction: Recent studies have shown acute cardioprotective effects of cyclosporine. The aim of the present study was to determine the protective role of cyclosporine on the model simulated the rotational nodal arrhythmia (AVNRT) by using extracellular field potential recordings of isolated atrioventricular-node (AV-node) of rabbit. Methods: This study was performed on isolated double-perfused AV-node of male New Zealand rabbits (1.5-2.5 kg) in one group (n=7). Basic and rate-dependent stimulation protocols (recovery, facilitation, fatigue) and arrhythmia threshold (index of refractoriness) and % Gap incidence were measured for assessment of electrophysiological properties of the AV- node. All stimulation protocols were repeated in control step and in the presence of various cumulative concentrations of cyclosporine (0.5 - 10 μm). Results: Cyclosporine prolonged the effective refractory period from 114.3±7.9 to 142±7.3 msec at the concentration of 10 μm. It also prolonged the functional refractory period from 162±3.3 to 178.6±5 msec and increased the time of Wenckebach at the concentrations of 5 - 10 μM. Various concentrations of cyclosporine increased fatigue and reached a significant level at 10 μm. Gap incidence was 82%, 16.6% and 20% in the control and treatments with 0.5 and 10 μm of cyclosporine, respectively. Conclusion: Block of MPTP by cyclosporine caused inhibition of basic and rate-dependent properties of atrioventricular node. Cyclosporine, by raising the threshold of arrhythmia, could be possibly considered as an anti- AVNRT drug.
Keywords: Atrio-ventricular node, Cyclosporine, Supraventricular Arrhythmia
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Type of Manuscript: Experimental research article | Subject: Cardiovascular Physiology/Pharmacology
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