Showing 8 results for Reperfusion
Anyamanesh S, Faghihi M, Kadkhodaei M,
Volume 61, Issue 2 (5-2003)
Abstract
During kidney and other organ transplantation, the organ to be transplanted, must inevitably remain out of the body with little or no blood perfusion at all for a long period of time (ischemia). These events have been suggested to cause the formation of oxygen- derived free radicals (OFR). Reperfusion (reintroduction of blood flow) will further exacerbate the initial damage caused by the ischemic insult and may result in the production of free radicals. The aim of this study was to investigate whether induction of brief periods of renal artery occlusion (ischemic preconditioning, IPC) can provide protection from the effects of a subsequent period of ischemia and reperfusion (IR) in the rat kidney.
Materials and Methods: In this regard, 28 white, male rats were randomly and equally divided into four groups: Control (sham- operated), IPC alone, IR alone (30 min ischemia followed by 10 min reperfusion), and IPC- IR. Preconditioning involved the sequential clamping of the right renal artery for 5 min and declamping for 5 min for a total of 3 cycles. To demonstrate the effectiveness of IPC regimen, vitamin E as an endogenous antioxidant and an index of lipid peroxidation was measured by HPLC after its extraction from right renal venous plasma and right renal tissue.
Results: Results of this study showed that the amount of vitamin E of renal tissue and venous plasma in the IR group had a significant decrease when compared to the control group (P< 0.0001). Whereas the amount of this vitamin in both renal tissue and venous plasma of the IPC- IR group was significantly higher than that in the IR group (P< 0.0001), but did not show any significant difference with the control group.
Conclusion: In this study, preconditioning method prevented the reduction of the endogenous antioxidant (Vit. E) in encountering the following sustained ischemic insult. Therefore, we suggest that ischemic preconditioning can be used to protect the Vit. E level of kidney from its subsequent decrease by ischemia and reperfusion.
P. Pasbakhsh, S. Saeednia, F. Abolhasani, M. Noori, M. Maphi, K. Mehran Nia, A Sobhani,
Volume 64, Issue 6 (8-2006)
Abstract
Background: The aim of this study was to determine the level of lipid peroxidation and tissue protein after superior mesenteric artery occlusion tissue damage. The effect of melatonin as anti oxidant and free radical scavenger in prevention of tissue damage, were also evaluated.
Methods: Thity six young male Wisatr-Albino rats (weight: 80-120 gr), were divided equally in 6 group with different concentrations of melatonin (10,20,30 mg/kg) treatment. Group 1was control, group 2 the sham that surgical process was applied until superior mesenteric artery dissection and received vehicle solution only in equally volume by intra muscular route. Group 3 was ischemia- reperfusion (I/R), group 4 was I/R plus melatonin 10 mg/kg, group 5 I/R plus melatonin 20 mg/kg and finally group 6 I/R plus melatonin 30 mg/kg. After laparatomy, a microvascular atraumatic clip was placed across the superior mesenteric artery under general anaesthesia and itbremoved after ischemia for 30 minutes. The first dose of melatonin was applied just beforereperfusion, second dose, after reperfusion and third dose on the second day .On third day rats were killed and their bowels were removed. The level of tissue melandialdehyde (MDA) as index of lipid peroxidation and tissue protein was determined.
Results: The level of tissue MDA were significantly lower in group 4, 5, 6 than group 3 (p<0.05). Tissue protein levels were significantly upper in group 4 than group 3. (p<0.001). There was no significant difference tissue protein level in group 5, 6 than group 3(p>0, 05).
Conclusion: These results suggest that melatonin 10 mg/kg has antioxidant effect in prevention of inducing tissue damage during SMA occlusion in rat intestine.
Kadkhodaee M, Golab F, Zahmatkesh M, Ghaznavi R, Hedayati M, Arab Ha, Soleimani M,
Volume 67, Issue 7 (10-2009)
Abstract
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Background: The effect of ischemia/reperfusion (I/R) injury on kidney has
been under investigation for many years. But the changes in liver function and
oxidative stress status in renal I/R injury is not well known. Recent studies
suggest a crosstalk between liver and kidneys. The aim of the present study was
to assess liver changes after induction of various degrees of renal I/R injury.
Methods: This is an
experimental study conducted on 20
male rats that were obtained from animal house of Physiology Department. Twenty
male rats were subjected to either sham operation or ischemia (30, 45 and 60 min) followed by 60 min reperfusion
periods. Blood samples were drawn post-operatively and plasma creatinine, BUN, ALT and AST were measured.
Hepatic glutathione (GSH) and FRAP (ferric reducing antioxidant power) levels and the concentration
of IL-10 and tumor necrosis
factor (TNF) -alpha were
evaluated.
Results: Both 45 and 60 min ischemia
followed by 1h reperfusion periods
resulted in significant increases in plasma creatinine (11.1±1.7mg/dl and 1.24±0.07mg/dl vs 0.55±0.15mg/dl, p<0.05) and BUN (34±3.85mg/dl and 35.0±2.81mg/dl vs 23.75±1.1mg/dl, p<0.05). These rats
showed a significant decrease in liver GSH as well as significant increase in TNF-a & IL-10 concentrations.
Conclusion: Renal ischemia causes
changes in liver function and oxidative stress status. A minimum of 45 min ischemia is needed to
study the effects of renal injury on liver as a remote affected organ.
Khansari M, Imani A, Faghihi M, Aali Anvari M, Moghimian M, Sadeghipour Roodsari Hr,
Volume 69, Issue 11 (2-2012)
Abstract
Background: Creatine kinase is a cardiac biomarker that is used for the assessment of ischemic injuries and myocardial infarction. The present study was designed to evaluate effects of oxytocin administration during ischemia and reperfusion periods on CK-MB levels in the coronary effluent of isolated rat heart and the possible role of oxytocin receptor, nitric oxide (NO), prostacyclin and mitochondrial ATP-dependent potassium channels in this regard.
Methods: Male wistar rats (n=8) were anesthetized with sodium thiopental and their hearts were transferred to a Langendorff perfusion apparatus. All animals were randomly divided into nine groups as follow in the ischemia-reperfusion group, hearts underwent 30 min of regional ischemia followed by 120 min of reperfusion. In oxytocin group, hearts were perfused with oxytocin 5 min after ischemia induction for 25 min. In other groups, 35 min prior to oxytocin perfusion, atosiban (a non-specific oxytocin receptor blocker), L-NAME (an NO synthase inhibitor), indomethacin (a non-specific cyclooxygenase blocker) and 5-HD (a specific mKATP channel blocker) were perfused for 10 min. In all groups, we measured CK-MB levels in the coronary effluent at the end of reperfusion. Moreover, coronary flow (mL/min) was measured at baseline, during ischemia period and 60 and 120 min after reperfusion.
Results: Oxytocin administration significantly reduced CK-MB level in oxytocin group as compared to ischemia-reperfusion group. Administration of atosiban, L-NAME, indomethacin and 5-HD prior to oxytocin perfusion abolished the effects of oxytocin on CK-MB levels.
Conclusion: Administration of oxytocin during ischemia and reperfusion periods deceased CK-MB levels but infusion of atosiban, L-NAME, 5-HD and indomethacin inhibited oxytocin from exerting its effects.
Gholampour F, Javadifar Ts, Karimi S, Eslam-Zadeh T, Owji Sm,
Volume 70, Issue 1 (4-2012)
Abstract
Background: Ischemia/reperfusion induced acute renal failure causes excretory functional disorders of nephrons. Ischemia/reperfusion injury is accompanied by generation of reactive oxygen species that leads to dysfunction, injury, and death of renal cells. Antioxidants of plant origin minimize the harmful effects of reactive oxygen species. The aim of this study was to determine the possible therapeutic potentials of Rosa canina L. in preventing renal functional disturbances during the post-ischemic reperfusion period.
Methods: In this experimental study undertaken for evaluating renal excretory function in 30 male Wistar rats, renal ischemia was induced by occluding both renal arteries for 45 min, followed by 24 h of reperfusion. The rats received 2 ml of tap water or a hydroalcoholic extract of Rosa canina (500 mg/kg) orally for 7 days before induction of ischemia. In plasma samples, creatinine and urea nitrogen levels were measured, and in renal tissue samples, red blood cells were counted. The data were analyzed using ANOVA and Duncan tests.
Results: Renal ischemia for 45 minutes increased plasma levels of creatinine (P<0.001) and nitrogen urea (P<0.01) while reducing red blood cell counts in renal glomeruli (P<0.001). Rosa canina administration diminished the increase in creatinine (P<0.001) and nitrogen urea concentrations (P<0.01), and prevented reductions in red blood cell counts in renal glomeruli (P<0.001).
Conclusion: Rosa canina seems to be useful as a preventive agent against renal damages induced by ischemia/reperfusion injuries in rats.
Kadkhodaee M, Khastar H, Seifi B, Najafi A, Delavari F,
Volume 70, Issue 2 (5-2012)
Abstract
Background: In a recent study, we were able to demonstrate a role for leukocyte transfer in the induction of liver damage in recipient mice after induction of IR (60 min of bilateral renal artery occlusion and 3 hrs reperfusion) injury in donors. The present study investigates the role of leukocyte transfer in the induction of kidney damage in recipient mice after induction of renal IR injury in donors.
Methods: Mice were divided into two sham and renal IR groups. After anesthesia, leukocytes were isolated from blood and were transferred to the two recipient groups: the intact recipient mice received leukocytes from the sham donor group (Sham recipient) and the intact recipient mice that received leukocytes from IR donor group (IR recipient). After 24 hrs, the recipient mice were anesthetized and blood samples and renal tissues were collected.
Results: Renal malondialdehyde (MDA) increased and glutathione and superoxide dismutase (SOD) decreased significantly in IR recipient group in comparison to sham recipient group. Although renal function tests, including BUN and plasma creatinine were significantly different between IR donor and sham donor groups, but they were not significantly different in two recipient groups. Renal tissues in IR donor group showed extensive damage compared to sham group, but in IR recipients' kidneys, they were different from IR donor tissues despite being different from their respective sham group.
Conclusion: These findings are suggestive of implication of leukocytes in renal tissue damage and oxidative stress after renal IR injury.
Behjat Seifi, Mehri Kadkhodaee , Enayatollah Bakhshi, Mina Ranjbaran , Parisa Ahghari , Bahareh Yasrebi ,
Volume 72, Issue 2 (5-2014)
Abstract
Background: The renal sympathetic nerve activity (RSNA) is enhanced in renal failure. Paraventricular nucleus in hypothalamus is an important central site to regulate sympathetic activity. There are angiotensin II (Ang) II receptors in this nucleus. The aim of this study was to evaluate the effects of angiotensin II in hypothalamic paraventricular nucleus (PVN) on renal ischemia-reperfusion injury and RSNA.
Methods: This study was done at 2013 in Physiology department of Tehran University of Medical Sciences. One week before the induction of renal Ischemia-Reperfusion (IR) in Sprague-Dawley rats, a cannula was inserted into the right PVN for microinjection of different doses of Ang II (3, 30, and 300 ng). Then right nephrectomy was done. After one week recovery, renal IR injury was induced by clamping the left renal artery for 45 minute and then reperfusion for 3 or 24 hour. Ten minutes before the induction of renal ischemia-reperfusion, administration of different doses of angiotensin II were done in different groups. In all animals, left renal sympathetic activity was recorded before and during renal ischemia. After 3 or 24 hours reperfusion the blood, kidney and brain were collected to assay renal function and histology and oxidative stress indices Superoxide Dismutase, SOD and Malondialdehyde, MDA) in PVN.
Results: Administration of different pharmacological doses of angiotensin II into PVN exaggerated the renal IR injury. Angiotensin II in different doses increased the plasma creatinine and BUN levels and renal histological markers in comparison to renal IR in-jury (P<0.05). Angiotensin II had detrimental effects on RSNA and oxidative stress in-dices Super Oxide Dismutase (SOD) and Malondialdehyde (MDA) in PVN as the dose was increased (P<0.05).
Conclusion: These data showed that the PVN is a responsive site for central Ang II-induced damage in renal IR injury. We suggested the central effects of Ang II in the PVN on renal IR injury are mediated by oxidative stress in the PVN, and the peripheral effects by a sympathetic pathway.
Fateme Azizi , Behjat Seifi , Mehri Kadkhodaee ,
Volume 75, Issue 9 (12-2017)
Abstract
Background: Renal ischemia reperfusion (RIR) injury is a common clinical syndrome that affects renal function and significantly increases morbidity and mortality. Hydrogen sulfide (H2S) is an endogenously gaseous mediator that exhibits many cytoprotective effects. Recently, studies have shown that H2S have opposite effects in different doses. Therefore, in the current study we investigated the effects of H2S at different doses on renal function after induced renal ischemia reperfusion injury model.
Methods: The present study is an experimental study in animals and was conducted in Tehran University of Medical Sciences in April 2014. Male Wistar rats were assigned to five main groups (n= 6): 1) Sham, 2) Ischemia reperfusion (IR), 3) Administration of 50 µmol/kg Sodium hydrosulfide (NaHS)+IR, 4) Administration of 75 µmol/kg NaHS+IR and 5) Administration of 125 µmol/kg NaHS+IR. Sham group underwent laparotomy without cross-clamping of renal pedicles. Renal ischemia (IR) was induced in rats by both renal arteries occlusion for 55 min followed by reperfusion. Rats in the NaHS groups received intraperitoneal injections of 50, 75, or 125 µmol/kg of NaHS 10 minutes before the onset of ischemia and immediately after the onset of reperfusion. After reperfusion, plasma was collected for functional evaluation.
Results: Compared to the sham, IR animals demonstrated a significant rise in plasma creatinine and BUN levels. Rats in the low-dose NaHS treated groups (H50, H75) had improved renal function by significantly decrease of creatinine and BUN levels. However, treatment with a high-dose of NaHS increased the levels of plasma creatinine and BUN levels as compared with these indices in the IR group.
Conclusion: Our study demonstrates that different doses of Sodium hydrosulfide (NaHS) can play diverse role in renal ischemia reperfusion injury. However, NaHS in the low-doses could protect the kidney from the RIR injury, in a higher dose NaHS exaggerated the renal function by increases plasma creatinine and BUN. Therefore, determining of the therapeutic doses of NaHS may be important in the protection of kidney from the RIR injury.
