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

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

Dynamic age-related changes of extracellular field potential of isolated AV-node of rabbit

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 μM). 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

Lack of electrophysiological remodeling of atrioventricular-node in isolated perfused cirrhotic rat during simulated atrial fibrilation

Objective: The present study is design to evaluate the protective electrophsiological role of Atrioventricular- Node (AV-Node) during laboratory simulated Atrial fibrillation in common bile-duct ligated (BDL) rats. Material and Methods : We compared the electrophysiological effects of cirrhosis in 18 isolated perfused rat heart randomly divided in 3 groups:1)sham 2)basic and rate dependent and 3)AF. Cirrhosis was induced by BDL for 6 weeks in rats. We used extracellular filed potential recording from upper atrium and right ventricular. The conduction time, refractoriness and frequency-dependent (Recovery, Facilitation and Fatigue) properties of AVNode were characterized by specific stimulation protocols. Experimental AF was simulated by high-rate atrial pacing with random coupling intervals (range 75/125 ms). All data shown as Mean ± SE. Results : Slow pathway conduction time and nbsp; and facilitation interval was prolonged in cirrhotic rats (78.8 ± 3.3 to 95.8 ± 4.2 ms in sham and cirrhotic rats, respectively). Nodal protective function during AF(R-R interval, concealed beats, ventricular refractoriness and zone of concealment) weren't affected by cirrhosis. Conclusion: Despite slow pathway conduction prolongation in cirrhotic rats, protective behavior of av-node didn't change after induction of cirrhosis

The influence of micro algae on corrosion of steel in fly ash geopolymer concrete: A preliminary study

Chloride is not the only main cause of corrosion of reinforced concrete structures in seawater environment. Microorganisms, such as bacteria and microalgae, in the seawater can induce microbiologically influenced corrosion (MIC) that leads to degradation of the concrete structures by formation of biofilm on the metallic surface. In this preliminary study, the impact of microalgae on the corrosion of steel reinforced bars in fly ash geopolymer concrete was studied. Corrosion potential, algae cells number, and pH measurement were carried out for fly ash geopolymer concrete and a control mix (Ordinary Portland Cement) samples. The results indicate that the corrosion potential of fly ash geopolymer concrete was influenced by the cathodic reaction during photosynthesis activities. The geopolymer concrete in algae-inoculated medium was found to be more tolerant to algal growth than the control mix (OPC concrete). There was a positive correlation between algae cell densities and the potential reading of the geopolymer

Acute effects of simvastatin to terminate fast reentrant tachycardia through increasing wavelength of atrioventricular nodal reentrant tachycardia circuit

Simvastatin (SV) leads to reduction of ventricular rhythm during atrial fibrillation on rabbit atrioventricular (AV) nodes. The aim of our study was (i) to determine the frequency-dependent effects of SV in a functional model, and (ii) to assess the effects of SV to suppress experimental AV nodal reentrant tachycardia (AVNRT). Selective stimulation protocols were used with two different pacing protocols, His to atrial, and atrial to atrial (AA). An experimental AVNRT model with various cycle lengths was created in three groups of perfused rabbit AV nodal preparations (n = 24) including: SV 3 μm, SV 7 μm, and verapamil 0.1 μm. SV increased nodal conduction time and refractoriness by AA pacing. Different simulated models of slow/fast and fast/slow reentry were induced. SV caused inhibitory effects on the slow anterograde conduction (origin of refractoriness) more than on the fast anterograde conduction time, leading to an increase of tachycardia cycle length, tachycardia wavelength and termination of slow/fast reentrant tachyarrhythmia. Verapamil significantly suppressed the basic and frequency-dependent intrinsic nodal properties. In addition, SV decreased the incidence of gap and echo beats. The present study showed that SV in a concentration and rate-dependent manner increased the AV effective refractory period and reentrant tachycardia wavelength that lead to slowing or termination of experimental fast AVNRT. The direction-dependent inhibitory effect of SV on the anterograde and retrograde dual pathways explains its specific antireentrant actions. © 2014 Société Française de Pharmacologie et de Thérapeutique

Protective role of simvastatin on isolated rabbit atrioventricular node during experimental atrial fibrillation model: Role in rate control of ventricular beats

The purpose of the present study was to determine (1) whether simvastatin (SV) modifies the ratedependent conduction time and refractoriness of the atrioventricular (AV) node and (2) how it can change the protective mechanism of the AV node during atrial fibrillation (AF). Predefined stimulation protocols were applied to detect the electrophysiological parameters of the AV node, including atrial-His conduction time, effective refractory period (ERP), functional refractory period (FRP), concealed conduction, excitable index, and fatigue in two groups of isolated, perfused rabbit AV nodal preparations (N016). The stimulation protocols (fatigue, recovery) were carried out during control and in the presence of SV (0.5, 0.8, 3, and 10 μM). Simulated AF was executed in a separate group (N08), and specific indexes, including H-H mean, zone of concealment (ZOC), and concealed beats were recorded. SV, in a concentration-dependent manner, prolonged ERP, FRP, and Wenckebach cycle lengths. It (10 μM) significantly increased fatigue and the excitable index. In addition, SV elicited prolongation of ZOC and H-H mean at 3 and 10 μM. SV-evoked prolongation of nodal refractoriness and concealed conduction caused ratedependent ventricular slowing effects during AF. The ability of simvastatin to decrease the excitable gap by its heterogeneous effects on nodal dual pathways proposes its protective role in AF. © Springer-Verlag 2012

Potentilla reptans L. postconditioning protects reperfusion injury via the RISK/SAFE pathways in an isolated rat heart

Background: Our previous study indicated that Potentilla reptans root has a preconditioning effect by its antioxidant and anti-apoptotic effects in an isolated rat heart ischemia/reperfusion (IR) model. In the present study, we investigated the post-conditioning cardio-protective effects of Potentilla reptans and its active substances. Methods: The ethyl acetate fraction of P. reptans root (Et) was subjected to an IR model under 30 min of ischemia and 100 min of reperfusion. To investigate the postconditioning effect, Et was perfused for 15 min at the early phase of reperfusion. RISK/SAFE pathway inhibitors, 5HD and L-NAME, were applied individually 10 min before the ischemia, either alone or in combination with Et during the early reperfusion phase. The hemodynamic factors and ventricular arrhythmia were calculated during the reperfusion. Oxidative stress, apoptosis markers, GSK-3β and SGK1 proteins were assessed at the end of experiments. Results: Et postconditioning (Etpost) significantly reduced the infarct size, arrhythmia score, ventricular fibrillation incidence, and enhanced the hemodynamic parameters by decreasing the MDA level and increasing expression of Nrf2, SOD and CAT activities. Meanwhile, Etpost increased the BCl-2/BAX ratio and decreased Caspase-3 expression. The cardioprotective effect of Etpost was abrogated by L-NAME, Wortmannin (a PI3K/Akt inhibitor), and AG490 (a JAK/STAT3 inhibitor). Finally, Etpost reduced the expression of GSK-3β and SGK1 proteins pertaining to the IR group. Conclusion: P. reptans reveals the post-conditioning effects via the Nrf2 pathway, NO release, and the RISK/SAFE pathway. Also, Etpost decreased apoptotic indexes by inhibiting GSK-3β and SGK1 expressions. Hence, our data suggest that Etpost can be a suitable natural candidate to protect cardiomyocytes during reperfusion injury. © 2021, The Author(s)

Preconditioning and anti-apoptotic effects of Metformin and Cyclosporine-A in an isolated bile duct-ligated rat heart

Despite all previous studies relating to the mechanism of cirrhotic cardiomyopathy (CCM), the role of cirrhosis on Ischemic Preconditioning (IPC) has not yet been explored. The present study strives to assess the cardioprotective role of IPC in bile duct ligated (BDL) rats as well as the cardioprotective role of Cyclosporin-A (CsA) and Metformin (Met) in CCM. Cirrhosis was induced by bile duct ligation (BDL). Rats� hearts were isolated and attached to a Langendorff Apparatus. The pharmacological preconditioning with Met and CsA was done before the main ischemia. Myocardial infarct size, hemodynamic and electrophysiological parameters, biochemical markers, and apoptotic indices were determined at the end of the experiment. Infarct size, apoptotic indices, arrhythmia score, and incidence of VF decreased significantly in the IPC group in comparison with the I/R group. These significant decreases were abolished in the IPC (BDL) group. Met significantly decreased the infarct size and apoptotic indices compared with I/R (BDL) and normal groups, while CsA led to similar decreases except in the level of caspase-3 and -8. Met and CsA decreased and increased the arrhythmia score and incidence of VF in the BDL groups, respectively. Functional recovery indices decreased in the I/R (BDL) and IPC (BDL) groups. Met improved these parameters. Therefore, the current study depicted that the cardioprotective effect of Met and CsA on BDL rats is mediated through the balance between pAMPK and apoptosis in the mitochondria. © 2020 Elsevier B.V