scholarly journals Combination effects of gallic acid and cyclosporine A during ischemia/ reperfusion on rat electrocardiogram parameters and arrhythmia

2021 ◽  
Vol 25 (2) ◽  
pp. 162-170
Author(s):  
Najmeh Sadeghi ◽  
◽  
Samira Saadatfard ◽  
Mahin Dianat ◽  
Hassanali Abedi ◽  
...  
Keyword(s):  
Gallic Acid ◽  
Cyclosporine A ◽  
Wistar Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Optimal Combination ◽  
Isolated Hearts ◽  
Isolated Myocardium ◽  
St Elevation ◽  
Control Sham

Introduction: Myocardial ischemia leads to electrical disturbance in the heart because of reactive oxygen specious. This study aimed to investigate the effects of gallic acid and cyclosporine A (CsA) together on electrocardiogram parameters in myocardium following ischemia - reperfusion (I/R) in isolated hearts. Methods: In this research, 50 Wistar rats weighing 250-300g were randomly divided into the 5 following groups: control, sham and gallic acid (7.5, 15 and 30mg/kg) in combination with CsA (0.2μM). On the eleventh day, the hearts were removed and perfused with Krebs solution and ischemia was induced for 30min. Then, cyclosporine was administered for 10min at the 10 minutes before reperfusion and 10 minutes the beginning of reperfusion. By placing the electrode, the parameters of RR, PR, QT, TpeakTend, JT and QTcB interval, ST elevation, R, P, Q, S, T amplitude were recorded before ischemia and during reperfusion. Results: This study showed that RR, JT, interval, p duration, ST elevation and PVC numbers of control were increased during ischemia compared with sham and decreased using gallic acid (7.5, 15 and 30mg/kg) in combination with CsA. In addition, P, R, S, T amplitude during the ischemia were decreased in control compared with sham and increased with gallic acid (15mg/kg) in combination with CsA. Conclusion: In conclusion, the optimal combination of both drugs decreased arrhythmia occurrence while increased electrical velocity of conduction and wave amplitudes in isolated myocardium after ischemia reperfusion injury.

scholarly journals Reducing Cardiac Injury during ST-Elevation Myocardial Infarction: A Reasoned Approach to a Multitarget Therapeutic Strategy

2021 ◽  
Vol 10 (13) ◽  
pp. 2968
Author(s):  
Alessandro Bellis ◽  
Giuseppe Di Gioia ◽  
Ciro Mauro ◽  
Costantino Mancusi ◽  
Emanuele Barbato ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Reperfusion Injury ◽  
Therapeutic Strategy ◽  
Ventricular Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
St Elevation Myocardial Infarction ◽  
Ischemic Time ◽  
St Elevation

The significant reduction in ‘ischemic time’ through capillary diffusion of primary percutaneous intervention (pPCI) has rendered myocardial-ischemia reperfusion injury (MIRI) prevention a major issue in order to improve the prognosis of ST elevation myocardial infarction (STEMI) patients. In fact, while the ischemic damage increases with the severity and the duration of blood flow reduction, reperfusion injury reaches its maximum with a moderate amount of ischemic injury. MIRI leads to the development of post-STEMI left ventricular remodeling (post-STEMI LVR), thereby increasing the risk of arrhythmias and heart failure. Single pharmacological and mechanical interventions have shown some benefits, but have not satisfactorily reduced mortality. Therefore, a multitarget therapeutic strategy is needed, but no univocal indications have come from the clinical trials performed so far. On the basis of the results of the consistent clinical studies analyzed in this review, we try to design a randomized clinical trial aimed at evaluating the effects of a reasoned multitarget therapeutic strategy on the prevention of post-STEMI LVR. In fact, we believe that the correct timing of pharmacological and mechanical intervention application, according to their specific ability to interfere with survival pathways, may significantly reduce the incidence of post-STEMI LVR and thus improve patient prognosis.

scholarly journals Preconditioning with L-alanyl-glutamine reduces hepatic ischemia-reperfusion injury in rats

2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 8-13 ◽  
Author(s):  
Raimundo José Cunha Araújo Júnior ◽  
Raimundo Gerônimo da Silva Júnior ◽  
Marcelo Pinho Pessoa de Vasconcelos ◽  
Sérgio Botelho Guimarães ◽  
Paulo Roberto Leitão de Vasconcelos ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Average Weight ◽  
Sham Operation ◽  
Hepatic Ischemia ◽  
Portal Triad ◽  
Hepatic Ischemia Reperfusion ◽  
Control Sham

PURPOSE: To evaluate the effects of pre-conditioning with L-alanyl- glutamine (L-Ala-Gln) in rats subjected to total hepatic ischemia. METHODS: Thirty Wistar rats, average weight 300g, were randomly assigned to 3 groups (n=10): G-1 - Saline, G-2- L-Ala-Gln, G-3-control (Sham). G-1 and G-3 groups were treated with saline 2.0 ml or L-Ala-Gln (0.75mg/Kg) intraperitoneally (ip) respectively, 2 hours before laparotomy. Anesthetized rats were subjected to laparotomy and total hepatic ischemia (30 minutes) induced by by clamping of portal triad. Control group underwent peritoneal puncture, two hours before the sham operation (laparotomy only). At the end of ischemia (G1 and G2), the liver was reperfused for 60 minutes. Following reperfusion blood samples were collected for evaluation of alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels. Liver (medium lobe) was removed for immunohistochemistry study with antibody for Caspase-3. RESULTS: It was found a significant decrease (p<0.05) of ALT levels (270.6 +40.8 vs 83.3 +5.5 - p <0.05), LDH (2079.0 +262.4 vs. 206.6 +16.2 - p <0.05) and Caspase-3 expression (6.72 +1.35 vs. 2.19 +1.14, p <0.05) in rats subjected to I / R, comparing the group treated with L-Ala -Gln with G-2. Also, the ALT level was significantly lower (P<0.05) in G-1 and G-2 groups than in G-3 (control group). CONCLUSION: L-Ala-Gln preconditioning in rats submitted to hepatic I/R significantly reduces ALT, LDH and Caspase-3 expression, suggesting hepatic protection.

scholarly journals Urinary N-Acetyl-Beta-D-Glucosaminidase Activity in Rat Experimental Ischemic and Toxic Models of Acute Kidney Injury

2017 ◽  
Vol 74 (1) ◽  
pp. 105
Author(s):  
Razvan Andrei CODEA ◽  
Mircea MIRCEAN ◽  
Sidonia Alina BOGDAN ◽  
Andras Laszlo NAGY ◽  
Alexandra BIRIS ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Experimental Model ◽  
Wistar Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Control Group ◽  
Tubular Injury ◽  
Group 2 ◽  
Group 1

The identification of a suitable prevention method which facilitates limiting the deleterious effects of acute kidney injuries is highly required. In order to identify a proper treatment for acute kidney injuries, a suitable experimental model that replicates the structural, metabolic and inflammatory lesions that occur in the natural acute injured kidney is highly necessary. Intense urinary NAG activity can be found in a variety of renal disease such as toxic nephropathies, ischemic renal injury following cardiac surgery or renal transplantation but also in glomerular disease especially in diabetic nephropathy. Rises in urinary NAG enzyme activity strongly suggests tubular cell damage and support NAG enzyme as a biomarker of renal tubular injury. The aim of this paper is to obtain a stable in vivo acute kidney injury experimental model, in Wistar, rats and to evaluate the urinary activity of N-acetyl-β-D-glucosaminidase (NAG) enzyme, blood levels of urea and creatinine and microstructural renal alterations induced by ischemia/reperfusion injury respectively gentamicin nephrotoxicity. For this purpose we have used a rat experimental model. Adult male Wistar rats weighing 250-300 g were randomly divided into 3 groups with 8 rats in each group. Group 1 served as a model for the renal ischemia/reperfusion injury experiment, group 2 served for toxic kidney injury experimental model and group 3 served as control group. All individuals in both groups 1 and 2 presented marked elevations in blood urea and creatinine at the moment of euthanasia (day 3 for group 1 and day 9 for group 2) compared to the control group where biochemical values remained within normal limits. Urine analysis of both group 1 and 2 showed marked urinary NAG index activity which suggests acute tubular injury, suggestion confirmed by histological evaluation of the renal parenchyma sampled from this subjects

scholarly journals Genetic Deletion or Pharmacological Inhibition of Soluble Epoxide Hydrolase Ameliorates Cardiac Ischemia/Reperfusion Injury by Attenuating NLRP3 Inflammasome Activation

2019 ◽  
Vol 20 (14) ◽  
pp. 3502 ◽  
Author(s):  
Ahmed M. Darwesh ◽  
Hedieh Keshavarz-Bahaghighat ◽  
K. Lockhart Jamieson ◽  
John M. Seubert
Keyword(s):  
Nlrp3 Inflammasome ◽  
Epoxide Hydrolase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Soluble Epoxide Hydrolase ◽  
Inflammasome Activation ◽  
Protective Effects ◽  
Isolated Hearts ◽  
Pyrin Domain ◽  
Cardioprotective Effects

Activation of the nucleotide-binding oligomerization domain-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome cascade has a role in the pathogenesis of ischemia/reperfusion (IR) injury. There is growing evidence indicating cytochrome p450 (CYP450)-derived metabolites of n-3 and n-6 polyunsaturated fatty acids (PUFAs) possess both adverse and protective effects in the heart. CYP-derived epoxy metabolites are rapidly hydrolyzed by the soluble epoxide hydrolase (sEH). The current study hypothesized that the cardioprotective effects of inhibiting sEH involves limiting activation of the NLRP3 inflammasome. Isolated hearts from young wild-type (WT) and sEH null mice were perfused in the Langendorff mode with either vehicle or the specific sEH inhibitor t-AUCB. Improved post-ischemic functional recovery and better mitochondrial respiration were observed in both sEH null hearts or WT hearts perfused with t-AUCB. Inhibition of sEH markedly attenuated the activation of the NLRP3 inflammasome complex and limited the mitochondrial localization of the fission protein dynamin-related protein-1 (Drp-1) triggered by IR injury. Cardioprotective effects stemming from the inhibition of sEH included preserved activities of both cytosolic thioredoxin (Trx)-1 and mitochondrial Trx-2 antioxidant enzymes. Together, these data demonstrate that inhibiting sEH imparts cardioprotection against IR injury via maintaining post-ischemic mitochondrial function and attenuating a detrimental innate inflammatory response.

Blocking Na+/H+ exchange reduces [Na+]i and [Ca2+]i load after ischemia and improves function in intact hearts

2001 ◽  
Vol 281 (6) ◽  
pp. H2398-H2409 ◽  
Author(s):  
Jianzhong An ◽  
Srinivasan G. Varadarajan ◽  
Amadou Camara ◽  
Qun Chen ◽  
Enis Novalija ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ringer Solution ◽  
Left Ventricular ◽  
Isolated Hearts ◽  
Intracellular Ca ◽  
Ionic Basis

We determined in intact hearts whether inhibition of Na+/H+ exchange (NHE) decreases intracellular Na+ and Ca2+ during ischemia and reperfusion, improves function during reperfusion, and reduces infarct size. Guinea pig isolated hearts were perfused with Krebs-Ringer solution at 37°C. Left ventricular (LV) free wall intracellular Na+ concentration ([Na+]i) and intracellular Ca2+ concentration ([Ca2+]i) were measured using fluorescence dyes. Hearts were exposed to 30 min of ischemia with or without 10 μM of benzamide (BIIB-513), a selective NHE-1 inhibitor, infused for 10 min just before ischemia or for 10 min immediately on reperfusion. At 2 min of reperfusion, BIIB-513 given before ischemia decreased peak increases in [Na+]i and [Ca2+]i, respectively, from 2.5 and 2.3 times (controls) to 1.6 and 1.3 times preischemia values. At 30 min of reperfusion, BIIB-513 increased systolic-diastolic LV pressure (LVP) from 49 ± 2% (controls) to 80 ± 2% of preischemia values. BIIB-513 reduced ventricular fibrillation by 54% and reduced infarct size from 64 ± 1% to 20 ± 3%. First derivative of the LVP, O2 consumption, and cardiac efficiency were also improved by BIIB-513. Similar results were obtained with BIIB-513 given on reperfusion. These data show that Na+ loading is a marker of reperfusion injury in intact hearts in that inhibiting NHE reduces Na+ and Ca2+ loading during reperfusion while improving function. These results clearly implicate the ionic basis by which inhibiting NHE protects the guinea pig intact heart from ischemia-reperfusion injury.

scholarly journals Hepatoprotective effect of sodium (S)-2-hydroxyglutarate against ischemia-reperfusion injury in Wistar rats

2020 ◽  
Vol 19 ◽  
pp. 8
Author(s):  
E. Cienfuegos-Pecina ◽  
D.P. Moreno-Peña ◽  
L. Torres-González ◽  
D. Garza-Villarreal ◽  
O.H. Mendoza-Hernández ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Wistar Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatoprotective Effect

Effects of intracoronary melatonin on ischemia–reperfusion injury in ST-elevation myocardial infarction

2014 ◽  
Vol 31 (1) ◽  
pp. 88-95 ◽  
Author(s):  
Sarah V. Ekeløf ◽  
Natalie L. Halladin ◽  
Svend E. Jensen ◽  
Tomas Zaremba ◽  
Jens Aarøe ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
St Elevation Myocardial Infarction ◽  
St Elevation
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