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Skeletal muscle ischemia and reperfusion in rats increase lipid peroxidation in rats
Piccinato, Carlos Eli;De Domenico Jr, Armando;Jord?o Jr, Alceu Afonso;Vannucchi, Helio;
Acta Cirurgica Brasileira , 2004, DOI: 10.1590/S0102-86502004000500018
Abstract: purpose: to determine the effects of 30 minutes of ischemia followed by 30 minutes of reperfusion in skeletal muscle of rats receiving three different diets (supplemented, normal and vitamin e deficient) on lipoperoxidation (lp). methods: lp measured by tbars levels, and plasma and hepatic concentrations of vitamin e measured by hplc. results: the deficient group presented higher lipoperoxidation levels in muscle compared to the control and supplemented groups. conclusion: supplementation with vitamin e decrease the free radicals production in ischemia/reperfusion in skeletal muscle of rats.
The protective effect of cilostazol on isolated rabbit femoral arteries under conditions of ischemia and reperfusion: the role of the nitric oxide pathway
Santos, Mariana R.G.A.;Celotto, Andréa C.;Capellini, Verena K.;Evora, Paulo R. B.;Piccinato, Carlos E.;Joviliano, Edwaldo E.;
Clinics , 2012, DOI: 10.6061/clinics/2012(02)13
Abstract: objectives: the clinical significance of ischemia/reperfusion of the lower extremities demands further investigation to enable the development of more effective therapeutic alternatives. this study investigated the changes in the vascular reactivity of the rabbit femoral artery and nitric oxide metabolites under partial ischemia/ reperfusion conditions following cilostazol administration. methods: ischemia was induced using infrarenal aortic clamping. the animals were randomly divided into seven groups: control 90 minutes, ischemia/reperfusion 90/60 minutes, control 120 minutes, ischemia/reperfusion 120/90 minutes, cilostazol, cilostazol before ischemia/reperfusion 120/90 minutes, and ischemia 120 minutes/cilostazol/ reperfusion 90 minutes. dose-response curves for sodium nitroprusside, acetylcholine, and the calcium ionophore a23187 were obtained in isolated femoral arteries. the levels of nitrites and nitrates in the plasma and skeletal muscle were determined using chemiluminescence. results: acetylcholine-and a23187-induced relaxation was reduced in the ischemia/reperfusion 120/90 group, and treatment with cilostazol partially prevented this ischemia/reperfusion-induced endothelium impairment. only cilostazol treatment increased plasma levels of nitrites and nitrates. an elevation in the levels of nitrites and nitrates was observed in muscle tissues in the ischemia/reperfusion 120/90, cilostazol/ischemia/reperfusion, and ischemia/ cilostazol/reperfusion groups. conclusion: hind limb ischemia/reperfusion yielded an impaired endothelium-dependent relaxation of the femoral artery. furthermore, cilostazol administration prior to ischemia exerted a protective effect on endotheliumdependent vascular reactivity under ischemia/reperfusion conditions.
Effect of N-acetylcysteine on lung injury induced by skeletal muscle ischemia-reperfusion: histopathological study in rat model
Sotoudeh, Amir;Takhtfooladi, Mohammad Ashrafzadeh;Jahanshahi, Amirali;Asl, Adel Haghighi Khiabanian;Takhtfooladi, Hamed Ashrafzadeh;Khansari, Mohammadreza;
Acta Cirurgica Brasileira , 2012, DOI: 10.1590/S0102-86502012000200012
Abstract: purpose: to investigate whether n-acetylcysteine, a free radicals scavenger has a protective effect against lung injury as a remote organ after skeletal muscle ischemia-reperfusion. methods: twenty wistar male rats were divided randomly into two experimental groups: group ischemia-reperfusion (group i) and group ischemia-reperfusion + n-acetylcysteine (group ii). all animals were undergone two hours of ischemia by occlusion femoral artery and 24h of reperfusion. before clamped the femoral artery, 250 iu heparin was administered via the jugular vein to prevent clotting. rats that were treated with n-acetylcysteine given iv at a dose of 150 mgkg-1, immediately before reperfusion. after 24h of reperfusion, animals were euthanized and left lung harvested for histopathological analysis under light microscopy. results: in the group i, tissues showed histological changes with intra-alveolar edema, intra-alveolar hemorrhage and neutrophilic infiltration. histopathologically, there was a significant difference (p = 0.005) between two groups. conclusion: administration of n-acetylcysteine treatment significantly decreased lung injury induced by skeletal muscle ischemia reperfusion according to histological findings.
Influence of ShuJinHuoXue Tablets on Ischemia Reperfusion Injury of Animals’ Skeletal Muscle  [PDF]
Zhihong Tong,Fang Yu,Zhonghua Liu,Haidong Liang
Molecules , 2012, DOI: 10.3390/molecules17078494
Abstract: Ischemia-reperfusion (IR) can lead to serious tissue oxidative injury in animals. ShuJinHuoXue tablet (SJHXT) is a Chinese Traditional Medicine which can relax the muscles and stimulate the blood circulation and has been used as a clinical medicine. In the present study, we investigated the effects of SJHXT pretreatment on oxidative injury using an animal model of acute limb IR. Results showed that SJHXT pre-treatment (200, 300 and 400 mg/kg/day) markedly reduced serum endothelin-1 (ET-1), thromboxane B2 (TXB2) levels and thromboxane B2/6-keto- prostaglandin F1α (TXB2/6-Keto-PGF1α), wet weight/dried weight (W/D) ratio, myeloperoxidase (MPO), creatine kinase (CK), lactate dehydrogenase (LDH) activities, and increased serum nitric oxide (NO), 6-Keto-PGF1α levels and NO/ET-1 ratio in the IR+SJHXT groups. In addition, the SJHXT pre-treatment (200, 300 and 400 mg/kg/day) markedly reduced skeletal muscle Ca2+, malondialdehyde (MDA) levels, increased Na+-K+-ATPase, Ca2+-Mg2+-ATPase, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. Our results suggest that SJHXT pre-treatment may improve skeletal muscle blood vessel microcirculation, decrease skeletal muscle oxidative injury and enhance antioxidant enzymes activities in IR animals.
Effect of Salvia leriifolia Benth. root extracts on ischemia-reperfusion in rat skeletal muscle
Hossein Hosseinzadeh, Azar Hosseini, Marjan Nassiri-Asl, Hamid-Reza Sadeghnia
BMC Complementary and Alternative Medicine , 2007, DOI: 10.1186/1472-6882-7-23
Abstract: Ischemia was induced using free-flap surgery in skeletal muscle. The aqueous and ethanolic extracts of S. leriifolia (100, 200 and 400 mg/kg) root and normal saline (10 ml/kg) were administered intraperitoneally 1 h prior reperfusion. During preischemia, ischemia and reperfusion conditions the electromyographic (EMG) potentials in the muscles were recorded. The markers of oxidative stress including thiobarbituric acid reactive substances (TBARS), total sulfhydryl (SH) groups and antioxidant capacity of muscle (using FRAP assay) were measured.In peripheral ischemia, the average peak-to-peak amplitude during ischemic-reperfusion was found to be significantly larger in extracts groups in comparison with control group. Following extracts administration, the total SH contents and antioxidant capacity were elevated in muscle flap. The MDA level was also declined significantly in test groups.It is concluded that S. leriifolia root extracts have some protective effects on different markers of oxidative damage in muscle tissue injury caused by lower limb ischemia-reperfusion.A vast amount of circumstantial evidence implicates oxygen-derived free radicals (especially superoxide and hydroxyl radical) and high-energy oxidants (such as peroxynitrite) are as mediators of inflammation, shock, and ischemia/reperfusion injury [1]. The oxidant injury can potentially occur during ischemia and reperfusion due to an excess production of oxygen free radicals, a decrease in antioxidant defenses, or both. Because antioxidants function by removing the toxic oxygen metabolites, they are generally highly effective in reducing ischemia-reperfusion injury [2]. Skeletal muscle ischemia and reperfusion injury remains an issue of concern because of the morbidity and mortality that follows revascularization of an acutely ischemic limb [3]. Many studies have suggested the beneficial antioxidant effects of antioxidant nutrients such as vitamin E, green tea extract, ginkgo biloba extract, resveratrol
Endothelium-dependent and -independent hepatic artery vasodilatation is not impaired in a canine model of liver ischemia-reperfusion injury
Miranda, L.C.;Viaro, F.;Ceneviva, R.;Evora, P.R.B.;
Brazilian Journal of Medical and Biological Research , 2007, DOI: 10.1590/S0100-879X2007000600016
Abstract: we investigated whether hepatic artery endothelium may be the earliest site of injury consequent to liver ischemia and reperfusion. twenty-four heartworm-free mongrel dogs of either sex exposed to liver ischemia/reperfusion in vivo were randomized into four experimental groups (n = 6): a) control, sham-operated dogs, b) dogs subjected to 60 min of ischemia, c) dogs subjected to 30 min of ischemia and 60 min of reperfusion, and d) animals subjected to 45 min of ischemia and 120 min of reperfusion. the nitric oxide endothelium-dependent relaxation of hepatic artery rings contracted with prostaglandin f2a and exposed to increasing concentrations of acetylcholine, calcium ionophore a23187, sodium fluoride, phospholipase-c, poly-l-arginine, isoproterenol, and sodium nitroprusside was evaluated in organ-chamber experiments. lipid peroxidation was estimated by malondialdehyde activity in liver tissue samples and by blood lactic dehydrogenase (ldh), serum aspartate aminotransferase (ast) and serum alanine aminotransferase (alt) activities. no changes were observed in hepatic artery relaxation for any agonist tested. the group subjected to 45 min of ischemia and 120 min of reperfusion presented marked increases of serum aminotransferases (alt = 2989 ± 1056 u/l and ast = 1268 ± 371 u/l; p < 0.01), ldh = 2887 ± 1213 iu/l; p < 0.01) and malondialdehyde in liver samples (0.360 ± 0.020 nmol/mgpt; p < 0.05). under the experimental conditions utilized, no abnormal changes in hepatic arterial vasoreactivity were observed: endothelium-dependent and independent hepatic artery vasodilation were not impaired in this canine model of ischemia/reperfusion injury. in contrast to other vital organs and in the ischemia/reperfusion injury environment, dysfunction of the main artery endothelium is not the first site of reperfusion injury.
Effects of Ascorbic Acid, Alpha-Tocopherol and Allopurinol on Ischemia-Reperfusion Injury in Rabbit Skeletal Muscle: An Experimental Study
Bilgehan Erkut, Ahmet zyaz c o lu, Bekir Sami Karapolat, Cevdet U ur Ko o ullar , Sait Keles, Azman Ate , Cemal Gundogdu, Hikmet Kocak
Drug Target Insights , 2012,
Abstract: Purpose: Ischemia reperfusion injury to skeletal muscle, following an acute arterial occlusion is important cause of morbidity and mortality. The aim of the present study was to determine and evaluate the effects of ascorbic acide, alpha-tocopherol and allopurinol on ischemia reperfusion injury in rabbit skeletal muscle. Methods: Forty-eight New Zealand white rabbits, all male, weighing between 2.5 to 3.0 (mean 2.8) kg, were used in the study. They were separated into four groups. Group I was the control group without any drugs. The other groups were treatment groups (groups II, III, and IV). Group II rabbits administrated 50 mg/kg ascorbic acide and 100 mg/kg alpha-tocopherol 3 days prior to ischemia, group III rabbits received 50 mg/kg allopurinol 2 days prior to ischemia, and group IV rabbits were administrated both 50 mg/kg ascorbic acide, 100 mg/kg alpha-tocopherol 3 days prior to ischemia and 50 mg/kg allopurinol 2 days prior to ischemia. Two hours ischemia and 2 hours reperfusion were underwent to the treatment groups. At the end of the reperfusion periods, muscle samples were taken from rectus femoris muscle for determination of superoxide dismutase, catalase and glutathione peroxidase activities as antioxidant enzymes, and malondialdehyde as an indicator of lipid peroxidation and xanthine oxidase levels as source hydroxyl radical. Besides, histopathological changes (edema, inflammation, ring formation and splitting formation) were evaluated in the muscle specimens. Results: In the treatment groups; superoxide dismutase (U/mgprotein), catalase (U/mgprotein), and glutathione peroxidise (U/mgprotein) levels increased, malondialdehyde (nmol/mgprotein) and xanthine oksidase (mU/mgprotein) levels decreased compared to control I (p < 0.05). Increase of superoxide dismutase, catalase, and glutathione peroxidase levels were the highest and decrease of malondialdehyde and xanthine oxidase levels were the highest in group IV compared to groups II and III, but no significant as statistically. Also amount of cellular injury in group II, III, and IV were lower than group I. Conclusions: Antioxidant medication may help lowering ischemia reperfusion injury. In our study, all drug medications are shown to be able to have an effective role for preventing ischemia reperfusion injury. Moreover, ascorbic acide + alphatocopherol + allopurinol group (group IV) may have a benefi cial effect to decrease the local and systemic damage due to ischemia-reperfusion injury.
Effects of Ascorbic Acid, Alpha-Tocopherol and Allopurinol on Ischemia-Reperfusion Injury in Rabbit Skeletal Muscle: An Experimental Study
Bilgehan Erkut,Ahmet ?zyaz?c?o?lu,Bekir Sami Karapolat,Cevdet U?ur Ko?o?ullar?
Drug Target Insights , 2007,
Abstract: Purpose: Ischemia reperfusion injury to skeletal muscle, following an acute arterial occlusion is important cause of morbidity and mortality. The aim of the present study was to determine and evaluate the effects of ascorbic acide, alpha-tocopherol and allopurinol on ischemia reperfusion injury in rabbit skeletal muscle.Methods: Forty-eight New Zealand white rabbits, all male, weighing between 2.5 to 3.0 (mean 2.8) kg, were used in the study. They were separated into four groups. Group I was the control group without any drugs. The other groups were treatment groups (groups II, III, and IV). Group II rabbits administrated 50 mg/kg ascorbic acide and 100 mg/kg alpha-tocopherol 3 days prior to ischemia, group III rabbits received 50 mg/kg allopurinol 2 days prior to ischemia, and group IV rabbits were administrated both 50 mg/kg ascorbic acide, 100 mg/kg alpha-tocopherol 3 days prior to ischemia and 50 mg/kg allopurinol 2 days prior to ischemia. Two hours ischemia and 2 hours reperfusion were underwent to the treatment groups. At the end of the reperfusion periods, muscle samples were taken from rectus femoris muscle for determination of superoxide dismutase, catalase and glutathione peroxidase activities as antioxidant enzymes, and malondialdehyde as an indicator of lipid peroxidation and xanthine oxidase levels as source hydroxyl radical. Besides, histopathological changes (edema, inflammation, ring formation and splitting formation) were evaluated in the muscle specimens. Results: In the treatment groups; superoxide dismutase (U/mgprotein), catalase (U/mgprotein), and glutathione peroxidise (U/mgprotein) levels increased, malondialdehyde (nmol/mgprotein) and xanthine oksidase (mU/mgprotein) levels decreased compared to control I (p < 0.05). Increase of superoxide dismutase, catalase, and glutathione peroxidase levels were the highest and decrease of malondialdehyde and xanthine oxidase levels were the highest in group IV compared to groups II and III, but no significant as statistically. Also amount of cellular injury in group II, III, and IV were lower than group I.Conclusions: Antioxidant medication may help lowering ischemia reperfusion injury. In our study, all drug medications are shown to be able to have an effective role for preventing ischemia reperfusion injury. Moreover, ascorbic acide + alphatocopherol + allopurinol group (group IV) may have a benefi cial effect to decrease the local and systemic damage due to ischemia-reperfusion injury.
Regulatory Mechanisms of Injury and Repair after Hepatic Ischemia/Reperfusion  [PDF]
Alex B. Lentsch
Scientifica , 2012, DOI: 10.6064/2012/513192
Abstract: Hepatic ischemia/reperfusion injury is an important complication of liver surgery and transplantation. The mechanisms of this injury as well as the subsequent reparative and regenerative processes have been the subject of thorough study. In this paper, we discuss the complex and coordinated responses leading to parenchymal damage after liver ischemia/reperfusion as well as the manner in which the liver clears damaged cells and regenerates functional mass. 1. Introduction Hepatic ischemia/reperfusion (I/R) injury is a consequence of vascular inflow occlusion due to portal vascular clamping during complex liver surgery. I/R injury of the liver is directly related to the duration of liver ischemia and is a major cause of morbidity and mortality from liver transplantation and resection [1–3]. There has been considerable study of the biochemical and cellular changes occurring during I/R which has informed clinical practice. The results of these studies, which are the focus of this paper, have led to advances in our understanding of the pathophysiology of hepatic I/R injury and the development of new therapeutic modalities. 2. Initiation of Reperfusion Injury Early work by Jaeschke et al. [4–6] established that there are two distinct phases of liver injury after warm I/R. The initial phase of injury occurring within the first couple of hours of reperfusion is characterized by Kupffer cell-induced oxidant stress. Kupffer cell production and release of reactive oxygen species, including superoxide anion and hydrogen peroxide, result in acute hepatocellular injury. Blockade of Kupffer cell activity, accomplished by administration of gadolinium chloride or methyl palmitate, reduces acute hepatocyte damage. In addition, complement activation products are critically important for Kupffer cell activation during the initial phase of injury as depletion of complement reduces Kupffer cell-induced oxidant stress [7]. Despite the contribution of Kupffer cell-derived oxidants, the extent of injury during this initial phase is far less than that observed at later time points. Events occurring during the initial phase of liver injury, including activation of Kupffer cells, initiate a complex inflammatory cascade leading to the recruitment of various populations of leukocytes to the liver. The first population of leukocytes recruited after reperfusion is CD4 T lymphocytes. 3. Hepatic Recruitment of CD4 T Cells Significant involvement of T lymphocytes in hepatic I/R was first demonstrated in 1997 in a report that found that T lymphocytes rapidly accumulated in the liver after
Crocus sativus L. (Saffron) Extract and its Active Constituents (Crocin and Safranal) on Ischemia-Reperfusion in Rat Skeletal Muscle  [PDF]
Hossein Hosseinzadeh,Mohammad Hadi Modaghegh,Zahra Saffari
Evidence-Based Complementary and Alternative Medicine , 2009, DOI: 10.1093/ecam/nem125
Abstract: Saffron and its constituents have been shown to decrease ischemia-reperfusion (I/R) injury in kidney or brain tissues. In this study, the effects of saffron ethanolic extract and its constituents, crocin and safranal, were evaluated in skeletal muscle during I/R injury. Hind limb ischemia was induced using clamping the common femoral artery and vein. After 2 h ischemia, the clamp of the femoral vessels of animals was taken off and the animal underwent 1h reperfusion. Muscle injuries were evaluated by recording of the electromyographic (EMG) potentials and performing some biochemical analysis including thiobarbituric acid reactive substances (TBARS), total sulfhydryl (SH) groups and antioxidant capacity of muscle (using FRAP assay). The ethanolic extract of saffron (5, 20 and 80 mg kg−1), crocin (50, 200 and 400 mg kg−1), safranal (0.1, 0.25 and 0.5 ml kg−1) and normal saline (10 ml kg−1) were administered intraperitoneally 1 h prior reperfusion. The average peak-to-peak amplitude during I/R was significantly increased in extract, crocin and safranal groups in comparison with control-ischemic group. Following saffron, crocin and safranal administration, the total SH contents and antioxidant capacity were elevated in muscle flap. The MDA level was declined significantly in test groups. It is concluded that saffron extract and its constituents show a protective effect against lower limb I/R in rat.
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