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Showing 8 results for Arrhythmias

Khalil Pourkhalili, Sohrab Hajizadeh, Ali Khoshbaten, Taki Tiraihi,
Volume 12, Issue 2 (8-2008)

Abstract Introduction: Resent studies have been shown beneficial effects of hyperoxia pretreatment against ischemia-reperfusion injury in different organs. The aim of the present study was to investigate early and late effects of normobaric hyperoxia (≥95% O2) pretreatment on ischemia-reperfusion injuries in isolated rat hearts. Methods: Following 60 and 180 minutes of hyperoxia, rat hearts were isolated immediately (H60 and H180) or 24 hours later (H60/24 and H180/24), and subjected to 30 minutes of regional ischemia followed by 120 minutes of reperfusion. Incidence and severity of ventricular arrhythmias, mechanical function of the heart and coronary flow were assessed during 120 min of reperfusion. LDH and CK release and infarct size were also assessed. Results: Incidence and severity of reperfusion arrhythmias significantly reduced by hyperoxia pretreatment, especially in the early phase of treanment. H180 reduced the incidence of ventricular fibrillation (VF) to 0% vs. 50% of normoxic control, p<0.05). VF duration decreased in H180 group (0 vs. 50±31s in the NC group, p<0.05) and duration of VT decreased in H60 and H180 groups compared to normoxic control group (NC) (1.5±0.7 s and 7.5±2.5 s vs. 17.7±3.3 s respectively, p<0.05). Hyperoxia improves mycardial contractile function and improves coronary flow during reperfusion. Infarct size and enzymes release were also significantly decreased in early and late phase of hyperoxia pretreatment. Conclusions: These results indicate that hyperoxia pretreatment before induction of regional heart ischemia reduces cardiac infarct size and attenuates reperfusion induced arrhythmias in isolated rat heart. Keywords: Hyperoxia, Ischemia-reperfusion injury, Heart protection, Arrhythmias
Vahid Khori, Fatemeh Alizadeh, Sorosh Aminosariyeh, Mona Pourabouk, Mohsen Nayebpour, Aref Salehi, Ahmadali Shirafkan, Saeid Saleki, Fakhri Badaghabadi, Ali Davariyan,
Volume 14, Issue 2 (7-2010)

Introduction: Recent evidence has indicated that statins can reduce the incidence of both supraventricular and ventricular arrhythmias with various mechanisms. The primary goal of the present study was to determine direct protective role of simvastatin in modifying concealed conduction and the zone of concealment in a simulated model of atrial fibrillation (AF) in an isolated atrioventricular (AV) node in rabbits. Methods: Male Newsland rabbits (1.5-2 kg) were used in all experiments. Stimulating protocols (recovery, AF, zone of concealment) were used to study electrophysiological properties of the node in one group (N=8). All of the stimulated protocols were repeated in the presence and absence of different doses of simvastatin (0.5-10 μm). Results were shown as mean ± S.E. Results: Significant inhibition of the basic properties of the AV node was observed after the addition of simvastatin. Significant prolongation of Wenkebakh index (wbcl) from 138.7±5.6 to 182.1±6.9 and functional refractory period (FRP) from 157.7±5.9 to 182.1±6 msec at the concentration of 10 μM was observed. Maximum efficacy of simvastatin in atrial fibrillation (AF) protocol was observed at the concentration of 3.10 μM, that was accompanied with prolonged HH interval and increased number of concealed beats. Zone of concealment significantly increased at the concentrations of 1.3 and 10 μM. Conclusion: This study shows the protective effect of simvastatin in the prolongation of ventricular beats during atrial fibrillation. The effect of simvastatin in increasing AV-nodal refractory period and zone of concealment are probably the anti-arrhythmic mechanisms of this drug.
Moslem Najafi, Afshin Gharakhani, Tahereh Eteraf Oskouei,
Volume 14, Issue 4 (1-2011)

Introduction: This study was aimed to investigate the effects of postconditioning by natural honey on cardiac arrhythmias in the ischemic isolated rat heart. Methods: Male Wistar rats were divided into four groups then anesthetized by sodium pentobarbital. The animal hearts were removed and quickly mounted on a Langendorff apparatus and perfused under constant pressure by a modified Krebs-Henseleit (K/H) solution that was previously equilibrated with 95% O2–5% CO2. The hearts were subjected to 30 min regional ischemia followed by 30 min reperfusion. In the control group, the hearts perfused by normal K/H solution, however in the postconditioning groups, they were perfused with natural honey (0.25, 0.5 and 1%) enriched K/H solution from 10 min before to 10 min after reperfusion. The ECGs were analyzed to determine the total number of ventricular ectopic beats (VEBs), ventricular tachycardia (VT), the incidence and duration of VT and ventricular fibrillation (VF) during last 10 min of ischemia and the first 30 min of reperfusion. Results: During ischemia, honey (0.25, 0.5 and 1%) produced significant reduction in the number of VEBs and number, duration and incidence of VT (P<0.01). The incidence and time spent in VF were lowered by honey compared to the control group (P<0.05). During reperfusion time, all used concentrations of honey significantly reduced the number of VEBs (P<0.05). In addition, honey (0.5 and 1%) decreased the number and duration of VT (P<0.01 and P<0.05, respectively). Moreover, VF duration was lowered by perfusion of honey (0.25 and 0.5 %) versus the control group (P<0.05). Conclusion: The results showed protective effects of postconditioning by honey against ischemia-reperfusion injuries as anti-arrhythmic activities. Probably, antioxidant activity of honey, by scavenging of free radicals, and the presence of important energy sources such as glucose and fructose by improvement of cardiac function may involve in these protective effects.
Fatemeh Safari, Sohrab Hajizadeh, Shahnaz Shekarforush, Mehdi Forouzandeh, Mohsen Foadoddini, Gholamreza Bayat, Bita Houshmand, Ali Khoshbaten,
Volume 15, Issue 1 (4-2011)

Introduction: Inhibition of renin angiotensin system represents an important approach in the management of cardiovascular diseases. The aim of this study was to explore the effects of pretreatment with non-hypotensive dose of angiotensin converting enzyme (ACE) inhibitor, ramiprilat and angiotensin type 1 (AT1) receptor blocker, losartan on myocardial infarct size and arrhythmias in a rat model of ischemia-reperfusion injury. Methods: Seventy male Wistar rats were divided into five groups. One group received saline as control. Other groups were given 10 mg/kg/day of losartan for one (L-1W) or ten weeks (L-10W) as well as 50 μg/kg/day of ramiprilat for one (R-1W) or ten weeks (R-10W) using a feeding needle. The rats were subjected to 30 minutes occlusion and 120 minutes reperfusion of the left coronary artery. Infarct size was determined using triphenyl tetrazolium chloride staining. Ischemia-induced ventricular arrhythmias were analyzed in accordance with the Lambeth conventions. Results: Myocardial infarct size and the number of ventricular beats were significantly reduced in R-1W group, but the reduction was not significant in L-1W. After increasing the duration of pretreatment to 10 weeks in L-10W group, the infarct size, the number of ventricular beats and the episodes of ventricular tachycardia were significantly decreased. However in R-10W group the reduction of ventricular arrhythmias was not significant Conclusion: Based on the above mentioned results it could be concluded that losartan and ramiprilat, at a nonhypotensive dose, can reduce the induction of arrhythmias and infarct size following myocardial ischemia reperfusion. These drugs appear to act in a time-dependent manner. Therefore, we expected an increased cardiac effect by long-term administration of losartan. However prolonged treatment with ramiprilat reduced its protective effect.
Shahnaz Shekarforush, Ali Noroozzadeh, Fatemeh Safari, Leila Golmanesh, Ali Khoshbaten,
Volume 15, Issue 2 (8-2011)

Introduction: It has been reported that traumas such as transverse abdominal incision before myocardial ischemia result in a significantly decreased infarct size. This phenomenon is named remote preconditioning of trauma. Since small skin burn is one of most common traumas, the effect of this injury on ischemia-induced arrhythmias and infarct size was investigated in a rat model of ischemia-reperfusion injury. Methods: Twenty-four male Wistar rats were randomly assigned to 3 groups. In burn and sham groups, less than 1% of total body surface area of the dorsal skin was exposed to 100 ˚C and 37 ˚C water, respectively. In ischemic preconditioning group, rats were exposed to one cycle of ischemia (5 min) and reperfusion (10 min). Ischemiareperfusion injury was induced with occlusion and release of left coronary artery for 30 and 120 min, respectively. Infarct size was measured using triphenyl tetrazolium chloride staining and arrhythmias were assessed in accordance with Lambeth conventions. Results: Infarct size was significantly reduced in ischemic preconditioning group compared with the sham group (27 ± 2% vs. 50 ± 5% P < 0.01). Infarct size in the burn group was not significantly reduced. Irreversible ventricular fibrillation was 50% of all ventricular fibrillation in the burn group, while it was 25% in the sham group, however, this difference was not significant. Conclusion: Acute minor coetaneous burn has neither protective nor harmful for the rat myocardial ischemiareperfusion injury.
Mahdih Faghihi , Ali Mohammad Alizadeh, Vahid Khori, Vahid Khodayari , Saeed Moradi ,
Volume 16, Issue 4 (1-2013)

Abstract Introduction: Occurrence of cardiac arrhythmias and myocardial infarction are two main deleterious events that are caused by ischemia-reperfusion (IR) injury in the heart. Cardiac preconditioning represents the most potent method of rescuing heart tissue from undergoing irreversible ischemic damage. The aim of the present study was to evaluate oxytocin (OT) cardioprotective effects and its signaling pathways in cardiac arrhythmias including ventricular tachycardia (VT) and ventricular fibrillation (VF) in anesthetized rats. Methods: Fifty-four rats were divided into nine groups. Animals’ hearts were subjected to 25 min ischemia and 2 h reperfusion. Oxytocin was used 25 min prior to ischemia. In certain groups, atosiban (an oxytocin receptor antagonist), atractyloside (an opener of mitochondrial permeability transition pore, mPTP) and N-acetylcysteine (a reactive oxygen species scavenger) were used 10 min prior to OT administration. Then, the severity and incidence of cardiac arrhythmias including VT and VF were measured. Results: OT administration significantly decreased the severity and incidence of cardiac arrhythmias compared to the IR group (P<0.05). Administration of atosiban, atractyloside and N-acetylcysteine abolished the cardiac preconditioning effect of OT in cardiac arrhythmia (P<0.05). Conclusion: The present study demonstrates that preconditioning with oxytocin reduced ischemia-reperfusioninduced ventricular arrhythmias and its signaling pathways are probably mediated through mitochondrial permeability transition pore and reactive oxygen species.
Vahid Khori , Ali Mohammad Alizadeh, Bagher Nikyar , Ardeshir Banikarimi, Fakhri Badaghabadi, Ahmad Soltani , Mohsen Nayebpour,
Volume 17, Issue 1 (3-2013)

Introduction: Endorphins are produced by cardiomyocytes, and exert different effects on the heart. The aim of the present study is to assess morphine effects on extracellular atrioventricular (AV) node field potential pattern and ventricular rhythm of isolated rabbit heart during experimental atrial fibrillation (AF). Methods: Effects of different concentrations of morphine (10, 20, 50 and 100 μM) were assessed by applying basic stimuli protocols involving Wenckebach, recovery, zone of concealment and concealed conduction parameters during experimental atrial fibrillation in isolated rabbit heart. Two-way ANOVA was used to compare the groups. Results: Morphine significantly suppressed basic parameters of AV node. Morphine (100 μM) significantly increased wenckebach index (153.6±3.9 to 169.8±2.9 ms) and functional refractory period (156.9±3.0 to 176.4±3.5 ms) (P<0.05). During experimental atrial fibrillation, morphine nonsignificantly increased mean His–His interval, concealed conduction and zone of concealment (P > 0.05). Conclusion: The present results showed that morphine has concentration-dependent effects on AV node electrophysiological properties. Morphine at low concentrations can decrease nodal conduction and refractoriness of AV node, but in high concentrations causes increased nodal conduction without concealed conduction changes. Dual effects of morphine can explain the unpredictable behavior of heart in cardiac tachyarrhythmias.
Vahid Khori, Habibeh Shirmohammali , Ali Mohammad Alizadeh, Maryam Rajaii, Ardeshir Banikarimi, Mohammadhadi Molseghi,
Volume 17, Issue 2 (7-2013)

Introduction: Cardiac preconditioning is an important method to reduce the damage caused by prolonged ischemia. Previous studies have shown that corticosteroids have protective effects on the heart, however at high concentrations this effect may be reduced with unknown mechanisms. We hypothesize that the contradictory effects of hydrocortisone at high concentration may be mediated via mineralocorticoid receptors. Therefore, this study was designed to determine the protective effects of various concentrations of hydrocortisone on the heart and its relationship with the mineralocorticoid receptor. Methods: In an experimental study, ninety-six male rats were divided into eight groups treated with different doses of hydrocortisone (1, 5, 10 and 20 μM). Spirinolactone was used as a mineralocorticoid receptor antagonist to investigate its role in the hydrocortisone acute effects on the heart. The hearts were excised first, and transferred and connected to the Langendorff system, and then subjected to 30 min ischemia and 90 min reperfusion. The infarct size and ventricular arrhythmias were measured. Two-way ANOVA was used to compare the groups. Results: The results showed that hydrocortisone at various concentrations could reduce the infarct size and protect cardiomyocytes. The protective effects were lower at high concentrations (P<0.05). Spironolactone, a mineralocorticoid receptor antagonist amplified these protective effects (P<0.05). Hydrocortisone and spironolactone administration not significantly decreased severity and incidence of ventricular arrhythmia in comparison with IR group (P>0.05). Conclusion: The results showed the hydrocortisone cardioprotective effects as a pharmacological preconditioning agent. Opposing effects of hydrocortisone at medium and high concentrations can at least be partially reversed by mineralocorticoid receptors.

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