scholarly journals Protective Role of Sulodexide on Renal Injury Induced by Limb Ischemia-Reperfusion

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Tao Yuan ◽  
Ni Yang ◽  
Wei Bi ◽  
Jinwen Zhang ◽  
Xueyan Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Sham Operation ◽  
Lipid Peroxidation Product ◽  
Histological Changes ◽  
Group I ◽  
Hk2 Cells

Background. Though widely known as a potent antithrombin agent with protective effects on the kidney and other remote organs, it is currently ambiguous when it comes to sulodexide’s function on ischemia-reperfusion (I/R) injury. With this research, we pursued to further explore how sulodexide exerts its influence on limb I/R injury, in which deleterious effects on the kidney were what we primarily focused on. Methods. We randomized twenty-four C57BL/6 male rats into three groups, namely, sham operation group (control group), I/R group, and sulodexide pretreatment group. Hematoxylin and eosin staining was applied for discovery of renal histological changes. Serum creatinine (Cr) and serum urea nitrogen (BUN) were measured. Apoptotic parameters were detected by the TdT-mediated dUTP Nick-End Labeling method. To what extent and levels that antiapoptotic and proapoptotic proteins were expressed could be sensitively revealed by immunohistochemistry assay. Lipid peroxidation product propylene glycol and inflammatory factors were examined by enzyme-linked immunosorbent assay. Additionally, an extracorporeal hypoxia-reoxygenation (H/R) model of human renal proximal tubule epithelial HK2 cells was established. Our targets lay in cell proliferation and apoptosis, and we used western blotting to reflect apoptosis-related gene expression. Results. The levels of serum BUN, Cr, and inflammatory factors in sulodexide-intervened rats manifested significant reduction when compared with the I/R group. Also, sulodexide could protect the kidney from histological changes and could effectively inhibit intraparenchymal apoptosis. Furthermore, adding 2 μl/mL or 5 μl/mL of sulodexide to H/R model cells in vitro gave rise to significant restoration of the degenerative proliferation capacity of the HK2 cells following H/R injury and late cellular apoptosis experienced dramatic reduction versus the H/R group. When treated with 5 μl/mL of sulodexide at a dose of 10 mg/kg, the levels of the antiapoptotic proteins were increased, while the proapoptotic proteins showed opposite trends. Notable escalation on antiapoptotic protein expression level, in contrast with the opposite trends exhibited in proapoptotic proteins, was observed with 5 μl/mL sulodexide pretreatment with the dosage being 10 mg/kg. Conclusion. Sulodexide can protect against kidney damage caused by I/R injury of the lower limbs by enhancing cell proliferation, inhibiting apoptosis, reducing inflammatory reactions, and scavenging oxygen free radicals.

scholarly journals The Effect of Erythropoietin on Ischemia/Reperfusion Injury after Testicular Torsion/Detorsion: A Randomized Experimental Study

ISRN Urology ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Fahimeh Kazemi Rashed ◽  
Babollah Ghasemi ◽  
Hamid Deldade Mogaddam ◽  
Mehran Mesgari
Keyword(s):  
Testicular Torsion ◽  
Ischemia Reperfusion Injury ◽  
Protective Efficacy ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Sham Operation ◽  
Scoring Method ◽  
Group Vi ◽  
Sham Operation Group ◽  
Group I

This study was conducted to investigate the protective effect of erythropoietin (EPO) on ischemia/reperfusion related changes after testicular torsion/detorsion. In a randomized experimental trial 30 male rats were randomly allocated into six equal groups of five rats each. Group I (orchiectomy for histopathologic examination), group II (sham operation), group III (torsion for 2 hours, and ischemia/detorsion for 24 hours, and orchiectomy); group IV (torsion for 2 hours, ischemia/detorsion for 24 hours with erythropoietin injection then orchiectomy), group V (torsion for 2 hours and detorsion and EPO injection and orchiectomy 1 week later, group VI (torsion for 2 hours/detorsion and orchiectomy 1 week later). Two groups (groups 4 and 5) received different protocols of erythropoietin administration after testicular torsion/distortion. other groups were not receiving erythropoietin. Johnsen’s spermatogenesis scoring method and Cosentino’s histologic staging method were used to assess main outcome measures of the study. After the experimentation, Johnsen’s score in EPO Groups was statistically different from the score in some groups not receiving erythropoietin. Cosentino’s score in EPO groups was statistically different from the score in all groups not receiving erythropoietin. Neovascularization, vascular necrosis, vascular congestion, edema, hemorrhage, and acute inflammation were observed in some groups. This study shows short-term protective efficacy of erythropoietin on rat testicular injury after ischemia/reperfusion.

scholarly journals THE EFFECT OF DEXAMETHASONE ON SPERMATOGONIUM AND SERTOLI CELL OF IPSILATERAL TESTIS IN UNILATERAL TESTICULAR TORSION WISTAR RAT

2018 ◽  
Vol 25 (2) ◽  
Author(s):  
Ferdyan Rachmat Efendi ◽  
Johan Renaldo ◽  
Tarmono Djojodimedjo
Keyword(s):  
Body Weight ◽  
Sertoli Cell ◽  
Sertoli Cells ◽  
Testicular Torsion ◽  
Wistar Rat ◽  
Male Rats ◽  
Sham Operation ◽  
Group I ◽  
Significant Difference ◽  
The Mean

Objective: To investigate the effect of dexamethasone on spermatogonium and sertoli cell of ipsilateral testis in unilateral testicular torsion strain wistar rat. Material & Method: Experimental study with post-test only control group design. The present  study was conducted on 30 Wistar male rats aged 10 – 12 weeks grouped into 5 groups. Group I was the normal/sham operation group (KN), group II was left testicular torsion for 4 hours group and followed  by manual detorsion  (K1), group III was left testicular torsion for 10 hours group and followed  by manual detorsion (K2),  group IV was left testicular torsion for 4 hours group and given dexamethasone 10 mg/kg body weight subcutaneously 30 minutes before manual etorsion (D1), and group V was left testicular torsion for 10 hours group and  given dexamethasone 10 mg/kg body weight subcutaneously 30 minutes before manual detorsion. All rats had left orchidectomy 4 hours after detorsion. The number of spermatogonium and sertoli cells were counted in histological seminiferous tubular testis that have obtained Haematoxylin Eosin staining. Data were analyzed by ANNOVA followed by Post Hoc Tukey for spermatogonium and Kruskal Wallis followed by Mann Whitney test for sertoli cell. Differences were considered significant at p <0.05. Results: There was significant difference in the mean number of spermatogonium between K1 & D1 group. Otherwise, there was no significant difference in the mean number of spermatogonium between K2 & D2. There was significant difference in the mean number of Sertoli cells between K1 & D1 group, likewise that between K2 & D2 group. Conclusion: These results suggest that dexamethasone has protective effect in spermatogonium and sertoli cell in testicular torsion for 4 hours.

scholarly journals Exosomes Mediate Hippocampal and Cortical Neuronal Injury Induced by Hepatic Ischemia-Reperfusion Injury through Activating Pyroptosis in Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Limei Zhang ◽  
Hanyu Liu ◽  
Lili Jia ◽  
Jingshu Lyu ◽  
Ying Sun ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neuronal Injury ◽  
Male Rats ◽  
Receptor Protein ◽  
Enzyme Linked Immunosorbent Assay ◽  
Hepatic Ischemia ◽  
Caspase 1 ◽  
Hepatic Ischemia Reperfusion

Background. The neuronal injury and cognitive dysfunction after liver transplantation have severe effects on the prognosis and life quality of patients. Accumulating evidence suggests that both exosomes and pyroptosis could participate in hepatic ischemia-reperfusion injury (HIRI) and play key roles in neuronal death. However, the link between exosomes and neuronal pyroptosis in HIRI awaits further investigation. Methods. After establishing the HIRI rat models, we primarily studied the role of pyroptosis in hippocampal and cortical neuron injury through detecting NOD-like receptor protein 3 (NLRP3), pro-caspase-1, cleaved-caspase-1, apoptosis-associated speck-like protein containing CARD (ASC), gasdermin D (GSDMD), interleukin-1beta (IL-1β), and interleukin-18 (IL-18) expressions with western blotting, immunohistochemical staining, and enzyme-linked immunosorbent assay (ELISA). Then, we intravenously injected normal male rats with exosomes isolated from the sera of HIRI-challenged rats and pretreated rats with MCC950, a specific inhibitor of NLRP3, and carried out the same assay. We also detected the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) in the hippocampal and cortical tissues. Results. The results indicated that NLRP3 inflammasome and caspase-1-dependent pyroptosis were activated in the hippocampus and cortex of HIRI rats. Furthermore, serum-derived exosomes from HIRI-challenged rats not only had the ability to cross the blood-brain barrier (BBB) but also had the similar effects on neuronal pyroptosis. Moreover, ROS and MDA productions were induced in the HIRI and exosome-challenged groups. In addition, to some degree, MCC950 could alleviate HIRI-mediated hippocampal and cortical neuronal pyroptosis. Conclusion. This study experimentally demonstrated that circulating exosomes play a critical role in HIRI-mediated hippocampal and cortical injury through regulating neuronal pyroptosis.

scholarly journals Long Non-coding RNAMALAT1 Knockdown Alleviates Cerebral Ischemia/Reperfusion Injury of Rats Through Regulating the miR-375/PDE4D Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Guangjian Zhang ◽  
Qingdong Wang ◽  
Daoqing Su ◽  
Yingliang Xie
Keyword(s):  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Factor ◽  
Pc 12 Cells ◽  
Lncrna Malat1 ◽  
Cerebral Ischemic

Objectives: Cerebral ischemic/reperfusion injury (CI/RI) is the clinical manifestation of cerebral ischemic stroke, which severely affects the health and life of the patients. We aimed to investigate the regulatory mechanism of long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on CI/RI in this study.Methods: The expression of lncRNA MALAT1 and miR-375 was detected by qRT-PCR. MTT was utilized to measure the viability of PC-12 cells. The levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and reactive oxygen species (ROS) were detected by LDH assay, SOD assay, and ROS assay, respectively. The apoptosis rate of PC-12 cells was measured by flow cytometry analysis. Through enzyme-linked immunosorbent assay, the levels of NF-α, IL-1β, and IL-6 were determined. The interactions between miR-375 and MALAT1/PDE4D were predicted by Starbase/Targetscan software and verified by the dual-luciferase reporter assay. Western blot assay was performed to determine the protein expression of Bcl-2, Caspase-3, and PDE4D.Results: LncRNA MALAT1 expression was highly upregulated in the middle cerebral artery occlusion (MCAO)/reperfusion (R) model of rats. Both MALAT1 downregulation and miR-375 upregulation reversed the inhibitory effect of oxygen and glucose deprivation (OGD)/R on cell viability and the promoting effects on LDH level, cell apoptosis, and inflammatory factors levels. MALAT1 targeted miR-375, whereas miR-375 targeted PDE4D. Overexpression of miR-375 attenuated OGD/R-induced injury in PC-12 cells by targeting PDE4D. Both the low expression of miR-375 and high expression of PDE4D reversed the promoting effect of MALAT1 knockdown on SOD level and the inhibitory effects on ROS level, inflammatory factor levels, and cell apoptosis.Conclusion: Suppression of MALAT1 alleviates CI/RI of rats through regulating the miR-375/PDE4D axis. This study provides a possible therapeutic strategy for human CI/RI in clinic.

scholarly journals Protease-Activated Receptor-1 Antagonist Protects Against Lung Ischemia/Reperfusion Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Shi-Jye Chu ◽  
Shih-En Tang ◽  
Hsin-Ping Pao ◽  
Shu-Yu Wu ◽  
Wen-I Liao
Keyword(s):  
Ischemia Reperfusion ◽  
Lung Epithelial Cells ◽  
Lung Model ◽  
Mitogen Activated Protein Kinase ◽  
Male Rats ◽  
Inflammatory Factors ◽  
Mouse Lung ◽  
Lung Edema ◽  
Chemokine Production ◽  
Mapk Pathways

Protease-activated receptor (PAR)-1 is a thrombin-activated receptor that plays an essential role in ischemia/reperfusion (IR)-induced acute inflammation. PAR-1 antagonists have been shown to alleviate injuries in various IR models. However, the effect of PAR-1 antagonists on IR-induced acute lung injury (ALI) has not yet been elucidated. This study aimed to investigate whether PAR-1 inhibition could attenuate lung IR injury. Lung IR was induced in an isolated perfused rat lung model. Male rats were treated with the specific PAR-1 antagonist SCH530348 (vorapaxar) or vehicle, followed by ischemia for 40 min and reperfusion for 60 min. To examine the role of PAR-1 and the mechanism of SCH530348 in lung IR injury, western blotting and immunohistochemical analysis of lung tissue were performed. In vitro, mouse lung epithelial cells (MLE-12) were treated with SCH530348 or vehicle and subjected to hypoxia-reoxygenation (HR). We found that SCH530348 decreased lung edema and neutrophil infiltration, attenuated thrombin production, reduced inflammatory factors, including cytokine-induced neutrophil chemoattractant-1, interleukin-6 and tumor necrosis factor-α, mitigated lung cell apoptosis, and downregulated the phosphoinositide 3-kinase (PI3K), nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways in IR-injured lungs. In addition, SCH530348 prevented HR-induced NF-κB activation and inflammatory chemokine production in MLE12 cells. Our results demonstrate that SCH530348 exerts protective effects by blocking PAR-1 expression and modulating the downstream PI3K, NF-κB and MAPK pathways. These findings indicate that the PAR-1 antagonist protects against IR-induced ALI and is a potential therapeutic candidate for lung protection following IR injury.

scholarly journals The effect of Liv-52 on liver ischemia reperfusion damage in rats

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Orhan Cimen ◽  
Hüseyin Eken ◽  
Ferda Keskin Cimen ◽  
Arif Burak Cekic ◽  
Nezahat Kurt ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Male Rats ◽  
Control Group ◽  
Sham Operation ◽  
Distilled Water ◽  
Liver Ischemia ◽  
Group Level ◽  
Healthy Group ◽  
Hepatoprotective Effects ◽  
Wistar Male Rats

Abstract Background Liver ischemia reperfusion (I/R) damage which is frequently seen in clinical hepatobiliary surgeries has no effective treatment for it. Liv-52, known to have hepatoprotective effects, is a natural antioxidant drug licensed by the Ministry of Health of India. The aim of our study is to investigate the effect of Liv-52 on liver damage induced by I/R in rats. Methods Albino Wistar male rats were divided into three groups; liver I/R (IR), 20 mg/kg Liv-52 + liver ischemia reperfusion (LIR) and sham operation applied to control group (HG). Liv-52 was administered to the LIR group (n = 6) 1 h prior to I/R application and distilled water was given orally to IR (n = 6) and HG (n = 6) groups as a solvent. Ischemia was determined as 1 h, and reperfusion was identified as 6 h in animals. Results Increased levels of alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase, malondialdehyde, myeloperoxidase, and decreased levels of superoxide dismutase, and glutathione related enzymes caused by I/R application have been converged to healthy group level with Liv-52 treatment and the damage in liver tissue has been improved histopathologically. Conclusions Liv-52 may be beneficial for preventing liver I/R damage in pre-surgery application.

scholarly journals The effect of Liv-52 on liver ischemia reperfusion damage in rats

2019 ◽  
Author(s):  
Orhan Cimen ◽  
Huseyin Eken ◽  
Ferda Keskin Cİmen ◽  
Arif Burak Cekic ◽  
Nezahat Kurt ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Male Rats ◽  
Control Group ◽  
Sham Operation ◽  
Distilled Water ◽  
Liver Ischemia ◽  
Group Level ◽  
Healthy Group ◽  
Hepatoprotective Effects ◽  
Wistar Male Rats

Abstract Background: Liver ischemia reperfusion (I/R) damage which is frequently seen in clinical hepatobiliary surgeries has no effective treatment for it. Liv-52, known to have hepatoprotective effects, is a natural antioxidant drug licensed by the Ministry of Health of India. The aim of our study is to investigate the effect of Liv-52 on liver damage induced by I/R in rats. Methods: Albino Wistar male rats were divided into three groups; liver I/R (IR), 20 mg/kg Liv-52 + liver ischemia reperfusion (LIR) and sham operation applied to control group (HG). Liv-52 was administered to the LIR group (n=6) one hour prior to I/R application and distilled water was given orally to IR (n=6) and HG (n=6) groups as a solvent. Ischemia was determined as one hour, and reperfusion was identified as six hours in animals. Results: Increased levels of alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase, malondialdehyde, myeloperoxidase, and decreased levels of superoxide dismutase, and glutathione related enzymes caused by I/R application have been converged to healthy group level with Liv-52 treatment and the damage in liver tissue has been improved histopathologically. Conclusions: Liv-52 may be beneficial for preventing liver I/R damage in pre-surgery application.

Effect of Edaravone on MicroRNA Expression in Exosomes after Hepatic Ischemia-reperfusion Injury

2021 ◽  
Vol 14 ◽  
Author(s):  
Yanxia Fei ◽  
Jiali Shao ◽  
Ge Huang ◽  
Lijuan Wang ◽  
Shuangfa Zou ◽  
...  
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Quantitative Polymerase Chain Reaction ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Hepatic Ischemia ◽  
Second Generation Sequencing ◽  
Hepatic Ischemia Reperfusion

Background and Objective: Hepatic ischemia-reperfusion injury (HIRI) results in serious complications after liver resection and transplantation. Edaravone (ED) has a protective effect on IRI. This study was designed to evaluate whether ED could protect the liver of rats from HIRI injury and explored its exosomal miRNA-related mechanism. Methods: The sham group, hepatic ischemia/reperfusion (IR group), and hepatic ischemia/reperfusion + edaravone (ED group) models were established. We determined the protective effect of ED by measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), superoxide dismutase (SOD); enzyme-linked immunosorbent assay for tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β); hematoxylin-eosin staining and immunohistochemistry for histopathological changes. Exosomal miRNAs were subjected to second-generation sequencing to identify their differential expression. The results were analyzed using bioinformatics methods and validated using real-time quantitative polymerase chain reaction (RT-qPCR). Results: HIRI rats showed higher levels of ALT, AST, oxidative stress, and inflammatory markers; ED attenuated these effects. The sequencing results showed 6 upregulated and 13 downregulated miRNAs in the IR vs. sham groups, 10 upregulated and 10 downregulated miRNAs in the ED vs. IR groups. PC-3p-190-42101 was screened as an overlapping differentially expressed miRNA, and RT-qPCR validation showed that its expression in HIRI rats was significantly decreased; ED prevented this downregulation. Moreover, the expression of PC-3P-190-42101 was significantly correlated with the level of inflammatory factors. Conclusion: These findings indicate that ED can regulate the level of inflammatory factors by affecting the expression of miRNA PC-3p-190-42101 in plasma exosomes to protect the liver from IRI.

scholarly journals Histological changes of the arterial bed of the hind limbs of the rats under condition of the acute ischemia-reperfusion and correction with the carbacetam

2020 ◽  
Vol 26 (2) ◽  
pp. 5-11
Author(s):  
T.O. Veresiuk ◽  
P.R. Selskyy ◽  
A.T. Televiak
Keyword(s):  
Histological Examination ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Acute Ischemia ◽  
Histological Changes ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Hind Limbs ◽  
Group I ◽  
Ischemic Period

The ischemic-reperfusion lesion is a complex multifactorial damage of the primary ischemic tissues as a result of restoration of the arterial blood circulation in them, which is accompanied by local morpho-functional reorganization of the vascular bed of the hind limbs of the rats. One of the promising means in the treatment and prevention of the reperfusion disorders is a carbacetam, which smooths the phenomena of hypo- and hyperperfusion in the post-ischemic period. The aim of the study was to established the manifestations of the morpho-functional remodeling of the vascular bed of the hind limbs of the rats in ischemia-reperfusion and under conditions of correction with carbacetam. Histological examination of the vascular bed of the hind limbs of 30 rats under conditions of ischemia-reperfusion (group I) and 30 rats in the simulation of ischemia-reperfusion, which in the post-ischemic period administered carbacetam once a day (5 mg/kg) for 14 days (group II) were done. There were 6 intact animals in the control group. Simulation of ischemia was performed by applying SWAT rubber tourniquets on the hind limbs for 2 hours, and reperfusion – by removing of the tourniquet. The animals of the experimental groups were divided into 5 subgroups with reperfusion terms after 1, 2 hours and 1 day, as well as after 7 and 14 days. Histological examination was performed according to generally accepted methods. The vascular bed in the middle third of the thigh and the shin below the tourniquet was examined using a Bresser Trino Researcher 40x–1000x microscope. Analyzing of the obtained results, was established that after 1 hour of the reperfusion the histological changes became a systemic, and after 1 day it were more significant. It should be noted that the thickness of the vessel walls increased, and the elastic membranes were partially eligned, thinned and torned. The stepwise clarity of the arterials walls structure was lost. The edema acquired a total nature. The histological examination of the vessels after 7 days revealed that the swelling of the walls decreased and the condition of the elastic frame was improved. There was a proliferation of collagen fibers in the adventitia, which was a response to ischemic effects. It is noted that after 14 days in all wall membranes the proliferative activity of fiboblasts was remained. Under the conditions of the correction with the carbacetam after 2 hours, the structural positive dynamics became more pronounced and increased to a maximum level after 7 days of the experiment. The number of the modified and exfoliated endothelial cells decreased, and the condition of smooth myocytes increased. Histologically, the gradual restoration of endothelial coverage of the intima was established. As follows, ischemia and reperfusion cause vascular remodeling after 1 hour with a peak of the manifestations after 1 day of the reperfusion, which includes edematous syndrome, dystrophic-degenerative changes with an inflammatory response to the damage, and in the late reperfusion period increased a fibroblasts activity. Gradual return of morphological changes occurs after 14 days of the experiment. Under the conditions of correction, the acceleration of the remodeling with stabilization of the process and the most possible structural restoration after 7 days of the study was noted.

scholarly journals Histological and biochemical serum effects of alpha-tocopherol on ischemia/reperfusion-related injuries induced in the pelvic limb of rats

2005 ◽  
Vol 20 (5) ◽  
pp. 375-381 ◽  
Author(s):  
Marcelo Gomes da Silva ◽  
Aldemar Araújo Castro ◽  
Eduardo Antonio Gonçalves Ramos ◽  
Ediriomar Peixoto ◽  
Fausto Miranda Jr ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Creatine Phosphokinase ◽  
Ischemia Reperfusion ◽  
Alpha Tocopherol ◽  
Male Rats ◽  
Control Group ◽  
Infrarenal Aorta ◽  
Arterial Blood ◽  
Group I ◽  
Group Ii

PURPOSE: To evaluate the protective action of alpha-tocopherol in ischemia/reperfusion injuries of pelvic member of rats. METHODS: Thirty adult male rats of the Wistar strain were randomized into three experimental groups of 10: Group I - control group with no ischemia or reperfusion. Groups II and III - four hours of ischemia and of hours of reperfusion by means of clamping of the infrarenal aorta. The animals of Group II were treated with saline and those of Group III were treated with i.v. alpha-tocopherol (50 mg/kg). Parameters studied were biopsies of the soleus muscle, dosing of creatine phosphokinase, lactate dehydrogenase, potassium, calcium and arterial blood gasometry. RESULTS: The results of biopsies of the soleus muscles studied by optical microscopy, were not significant in terms of presence of edema among the three groups studied. Variables inflammation and necrosis were not observed, therefore cannot be statistically analyzed. As to dosing of calcium and lactate dehydrogenase, the pH, pO2 and pCO2 values were not significant for all groups studied. We observed that the levels of potassium (Group II > Group I, Fcalculated = 5.84; Fcritical = 3.33), creatine phosphokinase (Group II > Groups I and III, Hcalculated = 13.92; Hcritical = 5.99) and bicarbonate (Groups I and III > Group II, Hcalculated = 11.98; Hcritical = 5.99) presented significant results among groups. CONCLUSION: From the serum biochemical perspective, the treatment with alpha-tocopherol has attenuated the metabolic injuries in the ischemia/reperfusion syndrome in this experimental model.

Sign in / Sign up

Export Citation Format

Share Document