scholarly journals Metabolites of Tryptophane and Phenylalanine as Markers of Small Bowel Ischemia-Reperfusion Injury

2018 ◽  
Vol 16 (1) ◽  
pp. 709-715
Author(s):  
Jana Mašlanková ◽  
Štefan Tóth ◽  
Vladimíra Tomečková ◽  
Tímea Tóth ◽  
Matan Katz ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Control Group ◽  
Serotonin Level ◽  
Vanillylmandelic Acid ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Hydroxyindoleacetic Acid

AbstractIschemic-reperfusion injury of the small intestine is an acute clinical condition with high mortality rate. This study describes the changes in levels of phenylalanine and tryptophan metabolites in intestinal homogenates and urine samples of Wistar male rats after 60 minutes of mesenteric ischemia and different reperfusion periods (1, 24, 30 hours) in comparison with a control group without the ischemia. The ischemic-reperfusion injury was quantified by the histopathological injury index. The levels of serotonin, epinephrine, and norepinephrine were determined in the intestinal homogenate and epinephrine, vanillylmandelic acid, and the 5-hydroxyindoleacetic acid was analyzed in urine using the HPLC method. The statistically significant increased level of serotonin, epinephrine and norepinephrine were detected in the intestinal samples after 24 hours of reperfusion (p<0.01); even the most elevated serotonin level was observed after one hour of reperfusion (p<0.001). A statistically significant decreased level of vanillylmandelic acid was observed after one hour of reperfusion, but it significantly increased after 24 hours (p<0.05) in urine. The elevated level of the 5-hydroxyindoleacetic acid after one hour and 24 hours after reperfusion (p<0.05) were determined in the urine. The most significant elevated epinephrine level was observed after 24 hours of reperfusion (p<0.001) in urine. Results showed a potential role of serotonin as an early biomarker (after one hour of reperfusion) of small intestinal damaged homogenate, while the best predictor of intestinal injury in urine was epinephrine, which was elevated after 24 hours.

scholarly journals Pretreatment Donors after Circulatory Death with Simvastatin Alleviates Liver Ischemia Reperfusion Injury through a KLF2-Dependent Mechanism in Rat

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Zhongzhong Liu ◽  
Xingjian Zhang ◽  
Qi Xiao ◽  
Shaojun Ye ◽  
Chin-Hui Lai ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Target Genes ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Control Group ◽  
Isolated Perfused Rat Liver ◽  
Enzyme Release ◽  
Circulatory Death ◽  
Dependent Mechanism

Objective. Severe hepatic ischemia reperfusion injury (IRI) can result in poor short- and long-term graft outcome after transplantation. The way to improve the viability of livers from donors after circulatory death (DCD) is currently limited. The aim of the present study was to explore the protective effect of simvastatin on DCD livers and investigate the underlying mechanism. Methods. 24 male rats randomly received simvastatin or its vehicle. 30 min later, rat livers were exposed to warm ischemia in situ for 30 min. Livers were removed and cold-stored in UW solution for 24 h, subsequently reperfused for 60 min with an isolated perfused rat liver system. Liver injury was evaluated during and after warm reperfusion. Results. Pretreatment of DCD donors with simvastatin significantly decreased IRI liver enzyme release, increased bile output and ATP, and ameliorated hepatic pathological changes. Simvastatin maintained the expression of KLF2 and its protective target genes (eNOS, TM, and HO-1), reduced oxidative stress, inhibited innate immune responses and inflammation, and increased the expression of Bcl-2/Bax to suppress hepatocyte apoptosis compared to DCD control group. Conclusion. Pretreatment of DCD donors with simvastatin improves DCD livers’ functional recovery probably through a KLF2-dependent mechanism. These data suggest that simvastatin may provide a potential benefit for clinical DCD liver transplantation.

scholarly journals Myocardial ischemic reperfusion injury – A review

2020 ◽  
Vol 11 (2) ◽  
pp. 1305-1311
Author(s):  
Elanthendral R ◽  
Gayathri K ◽  
Saravana Kumar S
Keyword(s):  
Myocardial Infarction ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Significant Rise ◽  
High Rate ◽  
Cell Swelling ◽  
Ischemic Reperfusion Injury ◽  
Ongoing Research ◽  
Ischemic Reperfusion

Myocardial ischemic reperfusion injury leads to the development of myocardial infarction and cardiovascular disease. Death due to these diseases is increasing at a high rate. Tissue damage due to ischemia and reperfusion results in the development of the above-mentioned diseases in heart. During prolonged ischemia, various physiological changes such as a decrease in ATP levels and intracellular pH occur due to dysfunction of ATP ase, and accumulation of lactate in myocardial tissue. The consequences of these reactions include increased accumulation of mitochondrial calcium, followed by cell swelling and death. Due to NF-kappa-B signal pathway activation and severe Cx43 degradation, a serious myocardial infarction occurs after ischemia/reperfusion injury. Knowledge related to the mechanism of ischemia-reperfusion injury and its related treatments is important. This review explains the prevalence, risk factors, mechanism, modern medicine and traditional medicine for myocardial ischemia-reperfusion injury. Numerous medicinal plants have been scientifically evaluated for cardioprotective activity. Herbs that have been reported to exhibit therapeutic potency against Ischemic reperfusion injury are discussed in detail. There are a lot of diseases that are caused due to ischemic perfusion injury and end up in a significant rise in the rate of mortality. The details about ongoing research related to new drug development against myocardial ischemic perfusion injury are discussed here.

scholarly journals Participation of Heart Mitochondria in Myocardial Protection Against Ischemia/Reperfusion Injury: Benefit Effects of Short-Term Adaptation Processes

2015 ◽  
pp. S617-S625 ◽  
Author(s):  
M. FERKO ◽  
I. KANCIROVÁ ◽  
M. JAŠOVÁ ◽  
I. WACZULÍKOVÁ ◽  
S. ČARNICKÁ ◽  
...  
Keyword(s):  
Infarct Size ◽  
Reperfusion Injury ◽  
Membrane Fluidity ◽  
Mitochondrial Membrane ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Favorable Effect ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Mitochondrial Membrane Fluidity

Acute streptozotocin diabetes mellitus (DM) as well as remote ischemic preconditioning (RPC) has shown a favorable effect on the postischemic-reperfusion function of the myocardium. Cardioprotective mechanisms offered by these experimental models involve the mitochondria with the changes in functional properties of membrane as the end-effector. The aim was to find out whether separate effects of RPC and DM would stimulate the mechanisms of cardioprotection to a maximal level or whether RPC and DM conditions would cooperate in stimulation of cardioprotection. Experiments were performed on male Wistar rats divided into groups: control, DM, RPC and DM treated by RPC (RPC+DM). RPC protocol of 3 cycles of 5-min hind limb ischemia followed by 5-min reperfusion was used. Ischemic-reperfusion injury was induced by 30-min ischemia followed by 40-min reperfusion of the hearts in Langendorff mode. Mitochondria were isolated by differential centrifugation, infarct size assessed by staining with 1 % 2,3,5-triphenyltetrazolium chloride, mitochondrial membrane fluidity with a fluorescent probe DPH, CoQ9 and CoQ10 with HPLC. Results revealed that RPC as well as DM decreased the infarct size and preserved mitochondrial function by increasing the mitochondrial membrane fluidity. Both used models separately offered a sufficient protection against ischemic-reperfusion injury without an additive effect of their combination.

Targeted disruption of peroxiredoxin 6 gene renders the heart vulnerable to ischemia-reperfusion injury

2006 ◽  
Vol 291 (6) ◽  
pp. H2636-H2640 ◽  
Author(s):  
Norbert Nagy ◽  
Gautam Malik ◽  
Aron B. Fisher ◽  
Dipak K. Das
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Wild Type ◽  
Ischemic Reperfusion Injury ◽  
Peroxiredoxin 6 ◽  
Ischemic Reperfusion

Peroxiredoxin 6 (Prdx6) is a novel peroxidase enzyme belonging to the Prdx family, which in mammals contains five more peroxiredoxins (Prdx1–Prdx5). Like glutathione peroxidase (GSHPx) and catalase, Prdx6 possesses H2O2-scavenging activities, and, like the former, it also removes hydroperoxides. Since significant amounts of catalase and GSHPx are present in the heart contributing toward the attenuation of H2O2 and hydroperoxides formed during ischemia-reperfusion injury and thereby providing cardioprotection, we asked whether Prdx6 also has any role in this process. In the present study we used Prdx6−/− mice to assess the role of Prdx6 in ischemic injury. Western blot analysis revealed the absence of any Prdx activity in the Prdx6−/− mouse heart, while the GSHPx-1 and catalase levels remained unchanged. Randomly selected hearts from Prdx6−/− mice and wild-type mice were subjected to 30 min of global ischemia followed by 120 min of reperfusion at normothermia. The hearts from the Prdx6−/− mice were more susceptible to ischemic reperfusion injury as evidenced by reduced recovery of left ventricular function, increased myocardial infarct size, and higher amount of apoptotic cardiomyocytes compared with wild-type mouse hearts. These Prdx6−/− hearts were also subjected to a higher amount of oxidative stress as evidenced by the presence of higher amount of malondialdehyde. The present study thus indicates a nonredundant role of Prdx6 in myocardial ischemic reperfusion injury as catalase, and GSHPx could not make up for the deficiency of Prdx6 activities.

scholarly journals Opioid Preconditioning Modulates Repair Responses to Prevent Renal Ischemia-Reperfusion Injury

2020 ◽  
Vol 13 (11) ◽  
pp. 387
Author(s):  
Adriana Franco-Acevedo ◽  
Raquel Echavarria ◽  
Bibiana Moreno-Carranza ◽  
Cesar-Ivan Ortiz ◽  
David Garcia ◽  
...  
Keyword(s):  
Renal Function ◽  
Reperfusion Injury ◽  
Tissue Repair ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Control Group ◽  
Vegf Receptor ◽  
Renal Hilum ◽  
Pharmacological Preconditioning

Progression to renal damage by ischemia-reperfusion injury (IRI) is the result of the dysregulation of various tissue damage repair mechanisms. Anesthetic preconditioning with opioids has been shown to be beneficial in myocardial IRI models. Our main objective was to analyze the influence of pharmacological preconditioning with opioids in renal function and expression of molecules involved in tissue repair and angiogenesis. Experimental protocol includes male rats with 45 min ischemia occluding the left renal hilum followed by 24 h of reperfusion with or without 60 min preconditioning with morphine/fentanyl. We analyzed serum creatinine and renal KIM-1 expression. We measured circulating and intrarenal VEGF. Immunohistochemistry for HIF-1 and Cathepsin D (CTD) and real-time PCR for angiogenic genes HIF-1α, VEGF, VEGF Receptor 2 (VEGF-R2), CTD, CD31 and IL-6 were performed. These molecules are considered important effectors of tissue repair responses mediated by the development of new blood vessels. We observed a decrease in acute renal injury mediated by pharmacological preconditioning with opioids. Renal function in opioid preconditioning groups was like in the sham control group. Both anesthetics modulated the expression of HIF-1, VEGF, VEGF-R2 and CD31. Preconditioning negatively regulated CTD. Opioid preconditioning decreased injury through modulation of angiogenic molecule expression. These are factors to consider when establishing strategies in pathophysiological and surgical processes.

Bardoxolone Ameliorates Cerebral Ischemia/ Reperfusion Injury in Male Rats

2019 ◽  
Vol 22 (04) ◽  
pp. 122-130
Author(s):  
Rihab H Al-Mudhaffer ◽  
Laith M Abbas Al-Huseini ◽  
Saif M Hassan ◽  
Najah R Hadi
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Favorable Effects of Astaxanthin on Brain Damage due to Ischemia- Reperfusion Injury

2020 ◽  
Vol 23 (3) ◽  
pp. 214-224 ◽  
Author(s):  
Esra Cakir ◽  
Ufuk Cakir ◽  
Cuneyt Tayman ◽  
Tugba Taskin Turkmenoglu ◽  
Ataman Gonel ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Brain Damage ◽  
Neurological Deficit ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Cortex Cell

Background: Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. Objective: The aim of this study was to investigate the role of ASX on brain IRI. Methods: A total of 42 adult male Sprague-Dawley rats were divided into 3 groups as control (n=14) group, IRI (n=14) group and IRI + ASX (n=14) group. Cerebral ischemia was instituted by occluding middle cerebral artery for 120 minutes and subsequently, reperfusion was performed for 48 hours. Oxidant parameter levels and protein degradation products were evaluated. Hippocampal and cortex cell apoptosis, neuronal cell count, neurological deficit score were evaluated. Results: In the IRI group, oxidant parameter levels and protein degradation products in the tissue were increased compared to control group. However, these values were significantly decreased in the IRI + ASX group (p<0.05). There was a significant decrease in hippocampal and cortex cell apoptosis and a significant increase in the number of neuronal cells in the IRI + ASX group compared to the IRI group alone (p<0.05). The neurological deficit score which was significantly lower in the IRI group compared to the control group was found to be significantly improved in the IRI + ASX group (p<0.05). Conclusion: Astaxanthin protects the brain from oxidative damage and reduces neuronal deficits due to IRI injury.

scholarly journals The protective effects of pomegranate extracts against renal ischemia-reperfusion injury in male rats

2014 ◽  
Vol 6 (1) ◽  
pp. 46 ◽  
Author(s):  
AhmetA Sancaktutar ◽  
MehmetN Bodakci ◽  
NamıkK Hatipoglu ◽  
Kemal Basarılı ◽  
Haluk Soylemez ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Male Rats ◽  
Protective Effects ◽  
Renal Ischemia Reperfusion Injury

scholarly journals The protective effect of L-arginine, tadalafil, and their combination in rat testes after ischemia and reperfusion injury

2017 ◽  
Vol 11 (1-2) ◽  
pp. 19 ◽  
Author(s):  
Gokhun Ozmerdiven ◽  
Burhan Coskun ◽  
Onur Kaygisiz ◽  
Berna Aytac Vuruskan ◽  
Burak Asiltas ◽  
...  
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Combination Group ◽  
Control Group ◽  
Ischemia And Reperfusion ◽  
Contralateral Testis ◽  
Treatment Groups ◽  
Testis Torsion

Introduction: Nitric oxide (NO) plays an important role in the ischemia and reperfusion process. In this study, we aimed to examine the effect of L-arginine, tadalafil, and their combination for preventionof the ischemia reperfusion injury after testis torsion in rats.Methods: A total of 40 adult, male Sprague-Dawley rats were allocated into five groups. Three hours of left testicular torsion was performed in each group, excluding the control group. While the ischemia reperfusion (I/R) group had no treatment, I/R + Arg group received L-arginine, I/R + Td group received tadalafil and I/R + Arg + Td group received tadalafil and L-arginine 30 minutes before the detorsion. Then the left testis was untwisted for four hours of reperfusion. After bilateral orchiectomy, lipid peroxidation (LPx) and glutathione (GSH) activities were examined in testicular tissue.Spermatogenesis was evaluated with Johnsen’s score.Results: LPx levels of the I/R group were found to be significantly higher than for groups that received drugs for both testes (p<0.001). GSH levels of the combination group were higher than I/R group inipsilateral testis (p<0.01) and it was significantly higher than other groups for contralateral testis (p<0.001 for I/R group, p<0.01 for I/R + Arg, p<0.05 for I/R + Td). Mean Johnsen’s score of the I/Rgroup was found to be significantly lower than treatment groups in ipsilateral testis (p<0.001 for I/R + Arg + Td group, p<0.01 for other treatment goups) and contralateral testis (p<0.001). The meanJohnsen score of the combination group was significantly higher than that of other treatment groups in ipsilateral testis (p<0.05) and it was significantly higher than in the I/R + Td group in the contralateral testis (p<0.05).Conclusions: L-arginine, tadalafil, and combination of these two molecules showed protective effect against ischemia/reperfusion injury for both testes after unilateral testis torsion.

scholarly journals Catalase activity as signal of antioxydant system affection under influence of limb ischemia-reperfusion

2021 ◽  
pp. 24-30
Author(s):  
Nataliya Volotovska
Keyword(s):  
Risk Factors ◽  
Blood Loss ◽  
Catalase Activity ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Mechanical Injury ◽  
Male Rats ◽  
Mechanical Trauma ◽  
Control Group ◽  
Ischemic Reperfusion

The use of hemostatic tourniquet is a proved means of primary care. However, systemic disorders, as well as ultrastructural, in the area of compression can significantly worsen the condition of the injured organism. The aim. Estimation of catalase level in rats’ liver on the background of modifications of ischemic-reperfusion syndrome to know the severest pathogenic combination for organism. Materials and methods. 260 white adult male rats were divided into 5 groups: control (KG), EG1 – simulation of isolated ischemia-reperfusion syndrome (IRS) of the limb, EG2 – simulation of isolated volumetric blood loss, EG3 – combination of IRS of the limb with blood loss, EG4 – simulation of isolated mechanical injury of the thigh, EG5 – combination of IRS of the limb and mechanical injury. The variability of catalase level in liver was analyzed. Results. It was found that each of the experimental interventions has led to changes of catalase activity in the liver. The most expressed pathological expressions were observed on the 3rd after interventions, when the studied index in EG3 was lower than in EG1 and EG2 in 6,2 times and by 33,1 %. On the 7th day catalase activity in EG3 was in 9,4 times and by 44,5 % times lower than in EG1 and in EG2 data concordantly. The combination of limb ischemia-reperfusion with blood loss in EG3 led to exhausting of liver antioxydant enzyme catalase in the most critical posttraumatic period (day 3). The same, but less significant effect was registered in the group of combination of mechanical trauma with ischemia-reperfusion in EG5. This proved the role of the tourniquet as a factor that complicated the course of traumatic disease due to ischemic reperfusion. Conclusions. In this experiment, founded risk factors of combination of ischemia-reperfusion with heavy blood loss emphasized the importance and particular attention on such widespread method of bleeding tratment, as the imposition of a tourniquet, as in our experiment it triggered risk factors of ischemia-reperfusion. It was shown katalase activity depression respectively to the periods of increasing of lipid peroxydation. There was peculiarity, that on the base of isolated IRS catalase activity was increased in 2,5 times comparely to control group, whereas the hardest depression of it was found on the background of IRS, combined with blood loss – catalase activity was lower, comparely to KG – in 2,5 times. The importance of understanding the suppression of hepatocytes’ antyoxydants is great, as it might help in prevention the development of liver failure or hepatorenal syndrome on the background of limb ischemia-reperfusion.

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