scholarly journals Renal ischemia and reperfusion injury: influence of chorpromazine on renal function and lipid peroxidation

2008 ◽  
Vol 23 (suppl 1) ◽  
pp. 42-46 ◽  
Author(s):  
Silvio Tucci Junior ◽  
Roberto Marins de Carvalho ◽  
Fábia Martins Celini ◽  
Adauto José Cologna ◽  
Haylton Jorge Suaid ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Renal Function ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Renal Ischemia ◽  
Control Group ◽  
Ischemia And Reperfusion Injury ◽  
Mda Content

PURPOSE: To evaluate the influence of chlorpromazine (CPZ) on renal function and lipid peroxidation in a rat model of kidney ischemia/reperfusion injury. METHODS: Forty eight Wistar rats underwent a laparotomy for hilar clamping of left kidney with a bulldog clamp for 60 minutes followed by organ reperfusion and contralateral nephrectomy. Of these, 26 received 3mg/kg of CPZ intravenously 15 minutes before renal ischemia (G-E) while the remaining 22 were used as ischemic control group (G-C). Eleven rats of G-E and 8 of G-C were followed for blood urea nitrogen and creatinine determinations before renal ischemia and at 1st, 4th and 7th postoperative days. Samplings of left renal tissue were obtained at 5 minutes (5 rats from each group) and 24 hours (9 G-C and 10 of G-E) of reperfusion for malondialdehy (MDA) content determination. Controls of renal MDA content were determined in kidneys harvested from 6 additional normal rats. RESULTS: Acute renal failure occurred in all animals but levels of BUN and creatinine were significantly lower in G-E (p<0.001). MDA content rose strikingly at 5 minutes of reperfusion in both groups (p>0.05) and returned near to normal levels 24 hours later. CONCLUSION: CPZ conferred partial protection of renal function to kidneys submitted to ischemia/reperfusion injury that seems to be not dependent on inhibition of lipid peroxidation.

scholarly journals Hydrogen sulfide treatment improves long-term renal dysfunction resulting from prolonged warm renal ischemia-reperfusion injury

2014 ◽  
Vol 8 (5-6) ◽  
pp. 413 ◽  
Author(s):  
Ian Lobb ◽  
Justin Zhu ◽  
Weihau Liu ◽  
Aaron Haig ◽  
Zhu Lan ◽  
...  
Keyword(s):  
Renal Function ◽  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Protective Effects ◽  
Ischemia And Reperfusion Injury ◽  
Renal Masses

Introduction: The incidence of renal cell carcinoma (RCC) continues to rise concurrently with the increased prevalence of end-stage renal disease worldwide. Treatment for small renal masses continues to be partial nephrectomy mostly involving the clamping of renal blood vessels. Although necessary, this technique results in warm renal ischemia and reperfusion injury (IRI) to the afflicted kidney. We have recently demonstrated that hydrogen sulfide (H2S), a novel endogenous gaseous molecule, protects against prolonged cold and short-term warm renal IRI. In the current study, we examined whether exogenous H2S has long-term protective effects against warm renal IRI associated with renal surgical procedures.Methods: Uni-nephrectomized Lewis rats underwent 1 hour of warm ischemia induced by clamping of the renal pelvis. Animals underwent either intraperitoneal treatment with phosphate buffered saline (PBS; IRI group) or PBS supplemented with 150 μM NaHS (H2S group), and were compared against Sham-operated rats.Results: H2S treatment improved long-term renal function as serum creatinine at day 7 was significantly decreased in the H2S group compared to IRI animals (p < 0.05). H2S treatment decreased the expression of pro-inflammatory markers TLR-4, TNF-α, IFNγ, IL-2and ICAM-1, increased the expression of pro-survival molecule Bcl-2 and decreased the expression of pro-apoptotic marker BID at postoperative day 1. H2S-treated kidneys also showed a significant decrease (p < 0.05) in infiltration of macrophages at day 7 post-IRI compared to no treatment.Conclusion: H2S treatment improved long-term renal function and decreased long-term inflammation associated with warm IRI, and may offer a novel therapeutic approach to preventing warm IRI-induced renal injury associated with renal surgical procedures.

scholarly journals Antioxidative and anti-inflammatory impact of valsartan against renal ischemia-reperfusion injury; role of nitric oxide signaling pathway

2019 ◽  
Vol 5 (2) ◽  
pp. e19-e19
Author(s):  
Leila Mohmoodnia ◽  
Sarina Safari Ahmadvand ◽  
Sahar Koushki ◽  
Behrooz Farzan ◽  
Sajad Papi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Renal Ischemia ◽  
Control Group ◽  
Type I ◽  
Angiotensin Receptor ◽  
Renal Ischemia Reperfusion Injury ◽  
Control Group Group

Introduction: Renal ischemia reperfusion injury is one of the main causes of acute renal failure, which is associated with high mortality. Tissue damage caused by ischemia-reperfusion occurs due to the release of oxygen free radicals. Type I angiotensin receptor antagonists such as valsartan can be useful in the treatment of chronic kidney disease and hypertension. Objectives: We aimed to evaluate the protective effect of valsartan against renal ischemia reperfusion via antioxidant property and nitric oxide (NO) signaling pathway. Materials and Methods: Fifty male Wistar rats (220±10 g) were randomly divided into five groups as follows: Group 1; healthy rats without ischemia-reperfusion (control group). Group 2; rats with ischemia reperfusion (IR) (IR control group). Group 3; rats with IR which received 30 mg/kg valsartan orally. Group 4; rats with IR which received 30 mg/kg valsartan together with 40 mg/kg L-NAME. Group 5; rats with IR which received 30 mg/kg valsartan together with 40 mg/kg L-arginine. To induce ischemia-reperfusion, rats were anesthetized with thiopental and underwent surgery. Then, we induced ischemia with blocking blood vessels for 45 minutes by clamping. Biochemical parameters including urea and creatinine were measured using commercial kits. Oxidative stress and inflammatory parameters were measured by ELISA method. Renal tissues were stained with hematoxylin and eosin. Finally, the Kolmogorov-Smirnov test was used to determine the normal distribution of data. Results: The findings of this study indicated that treatment with valsartan and valsartan plus L-arginine leads to significant decrease in the serum levels of creatinine, urea, and albumin/creatinine, malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in contrast to IR control group which has increased level of these parameters. On the other hand, treatment with valsartan and valsartan plus L-arginine lead to increase in the serum levels of glutathione peroxidase (GPX), in contrast to ischemia reperfusion control group. Conclusion: Our data revealed that valsartan as a type I angiotensin receptor antagonist could decrease oxidative stress and inflammation due to renal ischemia reperfusion injury. Hence, valsartan could propose as a therapeutic agent for kidney diseases such as renal ischemia-reperfusion injury regarded to these renoprotective effects.

scholarly journals Postconditioning ameliorates lipid peroxidation in liver ischemia-reperfusion injury in rats

2009 ◽  
Vol 24 (1) ◽  
pp. 52-56 ◽  
Author(s):  
Antonio Roberto Franchi Teixeira ◽  
Nilza T. Molan ◽  
Márcia Saldanha Kubrusly ◽  
Marta Bellodi-Privato ◽  
Ana Maria Coelho ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Blood Flow ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Liver Ischemia ◽  
Glutathione S Transferase ◽  
Ischemic Event

PURPOSE: Liver ischemia-reperfusion injury is a phenomenon presents in events like liver resections and transplantation. The restoration of blood flow may leads to local and systemic injury. Several techniques have been developed in order to avoid or ameliorate ischemia-reperfusion injury in clinical situations. The application of a sttuter reperfusion after the ischemic event (postconditioning) could alters the hydrodynamics and stimulates endogenous mechanisms that attenuate the reperfusion injury. The present study was designed to evaluate the potential protective effect of postconditioning in a model of ischemia-reperfusion in rats. METHODS: Hepatic anterior pedicle of median and left anterolateral segments were exposed and clamped for 1 hour. Two hours later, clamp was released in two different ways: Control Group (n=7): clamp was release straightforward; Postconditioning Group (n=7): clamp was released intermittently. Lipid peroxidation (malondialdehyde) and expression of the glutathione-s-transferase-α-3 gene were studied. RESULTS: Lipid peroxidation was significantly decreased in ischemic and non-ischemic liver by postconditioning. GST- α3 gene was overexpressed in postconditioned group, but not significantly. CONCLUSION: Postconditioning induced hepatoprotection by reducing lipid peroxidation in the ischemic and non-ischemic liver.

O2 metabolites cause reperfusion injury after short but not prolonged renal ischemia

1987 ◽  
Vol 253 (4) ◽  
pp. F685-F691 ◽  
Author(s):  
S. L. Linas ◽  
D. Whittenburg ◽  
J. E. Repine
Keyword(s):  
Renal Function ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Cellular Events ◽  
Perfusion Flow ◽  
Biochemical Assessment ◽  
Perfusion Flow Rate

Toxic O2 metabolites have been postulated to contribute to renal ischemia-reperfusion injury, but their biochemical assessment and contribution as a function of the duration of ischemia is unclear. To address this issue we measured renal function and renal cortical glutathione levels following 20, 30, or 45 min of ischemia in situ and then 60 min of reperfusion by the isolated kidney technique. Increasing durations of ischemia were associated with progressive decreases in perfusion flow rate, glomerular filtration rate, tubular Na reabsorption, and renal cortical glutathione following reperfusion. However, reperfusion following simultaneous addition of the permeable O2 metabolite scavenger dimethylthiourea (DMTU; but not urea) prevented glutathione consumption and attenuated reperfusion-induced injury after 20 and 30 min of ischemia. In contrast, reperfusion with DMTU prevented glutathione consumption but did not improve renal function after 45 min of ischemia. Similarly, reperfusion with dimethyl sulfoxide also attenuated renal injury after 20 and 30 min, but not after 45 min of ischemia. Thus reperfusion of kidneys made ischemic for 20 or 30 min is associated with decreases in tissue glutathione and renal function that were both inhibitable by addition of O2 metabolite scavengers during reperfusion. In contrast, addition of O2 metabolite scavengers during reperfusion of kidneys previously made ischemic for 45 min prevented decreases in glutathione but did not improve renal function. We conclude that O2 metabolites formed during reperfusion contribute to functional impairment in kidneys made ischemic for short durations up to 30 min) but that after prolonged ischemia (greater than 30 min) injury is primarily mediated by non-O2 metabolite-dependent cellular events.

scholarly journals Intravenously delivered mesenchymal stem cells prevent MVO formation after myocardial ischemia/reperfusion injury

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Xie
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Reperfusion Injury ◽  
Nk Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Group Versus ◽  
Control Group ◽  
Funding Source ◽  
Ischemia And Reperfusion Injury

Abstract   Microvascular obstruction (MVO) after primary PCI is identified as an independent risk factor for prognosis in AMI patients. Inflammatory response induced by ischemia and reperfusion injury (I/R injury) was considered as one of main mechanisms for MVO formation. Mesenchymal stem cells (MSCs) are a unique stromal cell type that confers immunomodulatory effect in cardiac disease. Here we investigate whether intravenously and immediately delivered MSC could be used as potential therapeutic method to attenuate MVO formation. A cardiac-catheterization-induced porcine model of myocardial I/R injury was established, and allograft MSCs were delivered intravenously and immediately. Cardiac magnetic resonance imaging was performed 2 days and 7 days after operation to determine infarct area, MVO and cardiac function. We observed that the animals with allograft MSC delivering revealed decreased MVO and infarct size, as well as improved LVEF. In histology analysis, decreased myocytes area, fibrosis and inflammatory cell infiltration were observed in peri-infarct zone of animals with allograft MSC delivering. Meanwhile, the concentrations of IL-6, CRP and IL-1β in the serum were reduced in the allograft MSC group versus the control group. Flow cytometry indicated that decreased NK cells in the peripheral blood and ischemic heart tissue in the animals with allograft MSC delivering. In summary, we observed that allograft MSC delivering intravenously and immediately after myocardium I/R injury could attenuate MVO formation in porcine by NK cells depression. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Natural Science Foundation of China

Ischemia-reperfusion reduces cystathionine-β-synthase-mediated hydrogen sulfide generation in the kidney

2009 ◽  
Vol 297 (1) ◽  
pp. F27-F35 ◽  
Author(s):  
Zhibin Xu ◽  
Gamika Prathapasinghe ◽  
Nan Wu ◽  
Sun-Young Hwang ◽  
Yaw L. Siow ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Kidney Tissue ◽  
Sprague Dawley ◽  
Transsulfuration Pathway

Cystathionine-β-synthase (CBS) catalyzes the rate-limiting step in the transsulfuration pathway for the metabolism of homocysteine (Hcy) in the kidney. Our recent study demonstrates that ischemia-reperfusion reduces the activity of CBS leading to Hcy accumulation in the kidney, which in turn contributes to renal injury. CBS is also capable of catalyzing the reaction of cysteine with Hcy to produce hydrogen sulfide (H2S), a gaseous molecule that plays an important role in many physiological and pathological processes. The aim of the present study was to examine the effect of ischemia-reperfusion on CBS-mediated H2S production in the kidney and to determine whether changes in the endogenous H2S generation had any impact on renal ischemia-reperfusion injury. The left kidney of Sprague-Dawley rat was subjected to 45-min ischemia followed by 6-h reperfusion. The ischemia-reperfusion caused lipid peroxidation and cell death in the kidney. The CBS-mediated H2S production was decreased, leading to a significant reduction in the renal H2S level. The activity of cystathionine-γ-lyase, another enzyme responsible for endogenous H2S generation, was not significantly altered in the kidney upon ischemia-reperfusion. Partial restoration of CBS activity by intraperitoneal injection of the nitric oxide scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide not only increased renal H2S levels but also alleviated ischemia-reperfusion-induced lipid peroxidation and reduced cell damage in the kidney tissue. Furthermore, administration of an exogenous H2S donor, NaHS (100 μg/kg), improved renal function. Taken together, these results suggest that maintenance of tissue H2S level may offer a renal protective effect against ischemia-reperfusion injury.

Morg1 heterozygous mice are protected from acute renal ischemia-reperfusion injury

2009 ◽  
Vol 297 (5) ◽  
pp. F1273-F1287 ◽  
Author(s):  
Elke Hammerschmidt ◽  
Ivone Loeffler ◽  
Gunter Wolf
Keyword(s):  
Transcription Factor ◽  
Reperfusion Injury ◽  
Renal Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Tubular Damage ◽  
Wild Type ◽  
Ischemia And Reperfusion Injury ◽  
Renal Ischemia Reperfusion Injury

Renal ischemia and reperfusion injury leads to acute renal failure when proinflammatory and apoptotic processes in the kidney are activated. The increase in hypoxia-inducible transcription factor-α (HIF-α), an important transcription factor for several genes, can attenuate ischemic renal injury. We recently identified a novel WD-repeat protein designated Morg1 (MAPK organizer 1) that interacts with prolyl hydroxylase 3 (PHD3), an important enzyme involved in the regulation of HIF-1α and HIF-2α expression. While homozygous Morg1 −/− mice are embryonic lethal, heterozygous Morg1 +/− mice have a normal phenotype. We show here that Morg1 +/− were partially protected from renal ischemia-reperfusion injury compared with wild-type Morg1 +/+ animals. Morg1 +/− mice compared with wild-type animals revealed a stronger increase in HIF-1α and HIF-2α expression in the ischemic-reperfused kidney associated with enhanced serum erythropoietin levels. However, no significant expression of HIF-1α and HIF-2α was found in nonischemic kidneys without any difference between Morg1 +/− and Morg1 +/+ mice. Ischemic kidneys of Morg1 +/− mice expressed more erythropoietin mRNA than ischemic kidneys from wild-type animals. Renal ischemia in Morg1 +/− mice resulted in a decrease in renal inflammation and reduction of proinflammatory cytokines (MCP-1, IP-10, MIP-2) compared with wild-type mice. Furthermore, there was significantly less apoptosis and tubular damage in Morg1 +/− kidneys after ischemia-reperfusion, and this was also reflected in significantly improved renal function compared with wild-type. Thus Morg1 may be a novel therapeutic target to limit renal injury after ischemia-reperfusion.

scholarly journals The effect of the antioxidant drug U-74389G on urea levels during ischemia reperfusion injury in rats

2017 ◽  
Vol 11 ◽  
Author(s):  
Constantinos Tsompos ◽  
Constantinos Panoulis ◽  
Konstantinos Toutouzas ◽  
Aggeliki Triantafyllou ◽  
George Zografos ◽  
...  
Keyword(s):  
Experimental Study ◽  
Renal Function ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Renal Ischemia

This experimental study examined the effect of the antioxidant drug U-74389G, on a rat model and particularly in a renal ischemia - reperfusion protocol. The effects of that molecule were studied biochemically using blood mean urea levels. Forty rats of mean weight 231.875 g were used in the study. Urea levels were measured at 60 min of reperfusion (groups A and C) and at 120 min of reperfusion (groups B and D). The drug U-74389G was administered only in groups C and D. U-74389G administration significantly decreased the predicted urea levels by 11.35%+2.73% (P=0.0001). Reperfusion time non-significantly increased the predicted urea levels by 2.26%+3.29% (P=0.4103). However, U-74389G administration and reperfusion time together significantly decreased the predicted urea levels by 6.31%+1.70% (P=0.0005). U-74389G administration whether it interacted or not with reperfusion time has significant decreasing effect on the urea serum levels, reflecting a respective renal function augmentation.

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