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Showing 7 results for Moheimani

Vahid Khori, Alimohammad Alizadeh, Mahsa Niknam, Hamid Reza Moheimani, Hamid Yazdi, Mona Pourabouk, Fakhri Badaghabadi, Shima Changizi, Mryam Rajaei, Mohsen Nayebpour,
Volume 15, Issue 2 (Summer 2011)
Abstract

Introduction: Developmental changes in atrioventricular nodal conduction time and refractoriness have been shown in several studies. Prevalence of atrioventricular nodal reentrant tachycardia (AVNRT) is clearly age-dependent. The purpose of this study was to determine developmental changes of basic and frequency-dependent electrophysiological properties of the atrioventricular node (AV-node) in neonatal and adult rabbits. Methods: In this study, the effects of increasing age on the basic and rate-dependent properties of isolated perfused AV-node were analyzed in neonatal (2-week-old) and adult (12-week-old) New Zealand rabbits. Specific stimulation protocols of recovery, facilitation and fatigue were separately applied in each group (n=7). Unipolar extracellular field potential was recorded by a silver electrode (100 M). Results: The results showed that the basic nodal properties (ERP, FRP, WBCL and AHmax) were significantly shorter in neonates compared to the adult group. The magnitude of fatigue was also decreased in the neonatal group compared to control (18.9 ±3.3 vs. 11.1 ± 1.2 msec). Time constant of recovery of the adult group was significantly higher than the neonatal group (P<0.05). Conclusion: The results of this study showed that nodal basic and frequency-dependent properties are age-related and different developmental changes of slow and fast pathways are responsible for this behavior and may reveal the grater susceptibility of AVNRT in young adults compared to infants.
Vahid Khori, Sepideh Shariatnejad, Alimohammad Alizadeh, Hamidreza Yazdi, Mona Pourabouk, Fakhri Badaghabadi, Hamid Reza Moheimani, Shima Changizi, Maryam Rajee, Mohsen Nayebpour,
Volume 15, Issue 2 (Summer 2011)
Abstract

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.
Masoomeh Mazandarani, Fatemeh Hoseini, Akhtar Seifi, Hooman Bayat, Mona Pourabouk, Fakhri Badaghabadi, Maryam Rajaei, Hamidreza Moheimani, Vahid Khori,
Volume 15, Issue 3 (Fall 2011)
Abstract

Introduction: Considering the long traditional history of anti-inflammatory and anti-spasmodic effects of Matricria spices on the gastrointestinal system, the present study aimed to investigate the role of calcium channels and Histamine receptors in the inhibitory effects of hydroalcoholic dry extract of German chamomile (Matricaria recutita L.) on the isolated rabbit jejunum. Methods: All experiments were done on the isolated jejunum of New Zealand rabbits (1.8-2.5 kg). Dry extract of aerial parts of M. recutita was obtained by the maceration technique. The study was performed on two groups (n=6 in each group). In the first group, the effects of cumulative concentrations of M. recutita (3×10-3-1×10-2 mg/ml) on normal and K+-induced contractions (50 mM) of isolated jejunum were studied. In the second group, the inhibitory role of M. recutita ( 3 – 13×10-3 mg/ml) was evaluated in the presence and absence of histamine and cetrizine. In the presence and absence of 10 μM certizine, a histamine H1-antagonist, a concentration-dependent inhibitory effect of M. recutita extract in the range of 3-13×10-3 mg/ml was recorded the rabbit jejunum. Results: Results showed that EC50 of M. recutita in the absence and presence of K+ was 6.3×10-3 and 6.5×10- 3mg/ml, respectively. IC50 values for two concentrations of M. recutita (8×10-3 , 1×10-2 ) to abrogated contractive phase of Histamine was 9.55 × 10-6 and 1.57 × 10-6 μM. Cetrizine (10 μM) abolished inhibitory effects of M. recutita (IC50=3.6×10-3), (p< 0.001). Conclusion: Dry extract of matricaria recutita had inhibitory effects on the contractions of isolated rabbit jejunum. Calcium channels and histamine were involved in these antispasmodic effects.
Vahid Khori, Alimohammad Alizadeh, Ameneh Navaiyan, Mohsen Nayebpour, Mona Porabouk, Fakhri Badaghabadi, Shima Changizi, Maryam Rajaei, Hamidreza Moheimani, Hamidreza Yazdi,
Volume 15, Issue 3 (Fall 2011)
Abstract

Introduction: The aim of the present study was to determine direct effects of NO modulation on protective electrophysiological properties of atrioventricular node (AV node) in the experimental model of AF in rabbit. Methods: Isolated perfused rabbit AV nodal preparations were used in two groups. In the first group (N=7), LNAME (50μM) was applied. In the second group (N=12), different concentrations of L - argenine (250 μM - 5000 μM) were added to the solution. Programmed stimulation protocols were used to quantify AV nodal conduction time, refractoriness and zone of concealment. AF protocol was executed by software with coupling intervals (ranging from 75 – 125 msec). Results: L-NAME had depressive effects on basic AV nodal properties. L-Arginine (250μM) had direct inhibitory effects on nodal conduction time, Wenckebach and refractoriness. Significant increases in the number of concealed beats were induced by L-Arginine (500 μM ). Number of concealed beats were increased from 700.7 ± 33.7 to 763 ±21 msec (P<0.05). Trend of zone of concealment prolongation in a frequency-dependent model was abrogated by Larginine (250, 5000 μM). Conclusion: NO at low concentration (in the presence of L-NAME) had facilitatory role on AV nodal properties, but at high concentration (in the presence of L-arginine) enhanced protective role of AV node during AF. Biphasic modulatory role of NO may affect protective behavior of AV node during AF.
Vahid Khori, Samaneh Naeimipour, Alimohammad Alizadeh, Ali Haeri Rouhani, Mona Pourabouk, Fakhri Badaghabadi, Maryam Rajaei, Sepideh Shariatnezhad, Hamidreza Moheimani, Saeed Saleki, Mohammad Ali Zeyghami, Mohsen Nayebpour,
Volume 15, Issue 4 (Winter 2012)
Abstract

Introduction: Previous studies have indicated a relationship between MPTP pore and AV nodal rate-dependent properties. The aim of present study was to determine acute direct effects of cyclosporine on extracellular field potential of isolated rabbit AV node during experimental atrial fibrillation. Methods: In one group of male New Zealand rabbits (1.5-2.5 kg) cumulative concentrations of cyclosporine (0.5 – 10 m) were applied on isolated perfused atrio-nodal preparation (n=7). Extracellular field potential recording was sampled during specific stimulation protocols (recovery, zone of concealment and atrial fibrillation) in the presence of drug on electrophysiological properties of AV-node. Results: Cyclosporine significantly decreased the ventricular rate (HH mean) from 231.8 ± 5.7 to 277.4 ± 14.6 msec and functional refractory period during AF (AF FRP) from 138.3 ± 7.5 to 161.2 ± 10.31 msec in control and treated groups, respectively. Effective refractory period during AF (AF ERP) was significantly decreased by cyclosporine 10 mM compared to control group (p<0.05). Conclusion: Cyclosporine-evoked slowing ventricular heart rate during AF was induced by increasing functional refractoy period and ZOC. A possible mechanism can be through blocking of MPT pores.
Vahid Khori, Samaneh Naeimipour, Ali-Mohammad Alizadeh, Mona Pourabouk, Fakhri Badaghabadi, Maryah Rajaei, Sepideh Shariatnezhad, Hamidreza Moheimani, Saeed Saleki, Mohammadali Zeyghami, Mohsen Nayebpour,
Volume 16, Issue 1 (Spring 2012)
Abstract

Introduction: Intranodal pathways of atrioventricular (AV) node play a vital role in the delay of conduction time in response to various atrial inputs. The present study was aimed to determine the frequency-dependent electrophysiological properties of concealed slow pathway according to a functional model of isolated rabbit atrioventricular node preparation after fast pathway ablation. Methods: Experiments were carried out in rabbit isolated heart AV-nodal preparations (N=8) by superfused/perfused mode. Extracellular recording was carried out from transitional cells of posterior and anterior extension of AV-node and upper part of atrium and its bundle. Unipolar silver electrode (100 μm) and direct voltage (100-110 V) was applied to create AV-nodal fast pathway ablation. Results: Minimum conduction time (AHmin) was significantly increased after fast pathway ablation (p<0.05). Fast pathway ablation had no significant impact on fatigue phenomenon but significantly reduced facilitation value (p<0.05). Rate-dependency properties of concealed slow pathway were explained according to functional nodal model. Conclusion: The mathematical functional model accurately simulated frequency-dependent electrophysiological properties of concealed slow pathway after fast pathway ablation, but some modifications are necessary for accurate prediction of nodal behavior in various cycle lengths and in arrhythmia. Concealed slow pathway may be considered as a potential electrophysiological substrate of fatigue and facilitation phenomenon
Vahid Khori, Ali Mohammad Alizadeh, Hamidreza Moheimani, Delaram Shakiba, Soroosh Soroosh Aminolsharieh Najafi, Shahryar Alizadeh, Taghi Amiriyani, Ardeshir Banikarimi, Mahdi Zahedi, Mohamad Hadi Molseghi, Ahmadreza Dehpour,
Volume 17, Issue 1 (Spring 2013)
Abstract

Introduction: The present study is aimed to evaluate electrophysiological remodeling of atrioventricular (AV) node and ventricular conduction during experimental atrial fibrillation (AF) model in isolated heart of cirrhotic rats. Methods: Cirrhosis-induced electrophysiological remodeling was evaluated in 24 isolated retrogradely perfused rat hearts in 2 groups (control and cirrhotic). Cirrhosis was induced after 6 weeks of common bile duct ligation in rats. Extracellular filed potential was recorded from upper atrium and right ventricle. The conduction time, refractoriness and frequency-dependent properties of AV node were characterized by specific stimulation protocols. Experimental AF was simulated by high-rate atrial pacing with random coupling intervals (range 75–125 ms). Results: Nodal conduction time and ventricular responsiveness were significantly increased in the cirrhotic rats compared to the control (95.8 ± 4.2 ms vs. 78.8 ± 3.3 ms) (P< 0.05). Nodal protective function during AF was potentiated with increased R-R interval, concealed beats, ventricular refractoriness and zone of concealment in the cirrhotic group. Cirrhosis evoked rate–dependent ventricular conduction time shortening with different patterns during arrhythmia. Conclusion: Cirrhosis-induced electrophysiological remodeling was shown by increased AV nodal conduction and shortened ventricular conduction. This electrophysiological remodeling may be considered as a new manifestation of cirrhotic cardiomyopathy in the heart, which can change ventricular rhythm during arrhythmia.

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