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superoxide dismutase/blödning
Länken sparas på Urklipp
Sida 1 från 690 resultat
Reduction in oxidative stress by superoxide dismutase overexpression attenuates acute brain injury after subarachnoid hemorrhage via activation of Akt/glycogen synthase kinase-3beta survival signaling.
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Recent studies have revealed that oxidative stress has detrimental effects in several models of neurodegenerative diseases, including subarachnoid hemorrhage (SAH). However, how oxidative stress affects acute brain injury after SAH remains unknown. We have previously reported that overexpression of
Vitreal superoxide and superoxide dismutase after hemorrhagic injury: the role of invasive cells.
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It was previously reported that injection of whole blood or hemoglobin into the rabbit vitreous is followed by two periods of immigration of phagocytic cells. The first period occurs within the first few days, and the second at round 3 weeks after experimental injury. In this report, invasive cells
Effects of hemorrhagic shock and retransfusion on catalase and superoxide dismutase activities in rabbits.
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The effects of hemorrhagic shock and retransfusion on the activities of two endogenous antioxidant enzymes, catalase and superoxide dismutase, were studied in male New Zealand white rabbits. Following instrumentation and stabilization, blood was withdrawn to reduce mean arterial pressure to 35 mmHg
The effect of vasoactive intestinal peptide (VIP) on superoxide dismutase and catalase activities in renal tissues of rats exposed to hemorrhagic ischemia-reperfusion.
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The effect of vasoactive intestinal peptide (VIP) on the activities of superoxide dismutase and catalase was investigated in renal tissues of rats exposed to 30% hemorrhage followed by reperfusion. In addition to enzyme activities, renal tissues were also histologically evaluated. Thirty percent
Gene transfer of extracellular superoxide dismutase failed to prevent cerebral vasospasm after experimental subarachnoid hemorrhage.
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OBJECTIVE
We examined the therapeutic effect of human extracellular superoxide dismutase (ECSOD) gene transfer in the prevention of delayed cerebral vasospasm after experimental subarachnoid hemorrhage (SAH) because it was reported ECSOD relieved early-stage vasospasm.
METHODS
Twenty mongrel dogs
Extracellular superoxide dismutase attenuates lung injury after hemorrhage.
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Reperfusion of the lung after hemorrhage generates free radicals such as superoxide (O(2)(.)) that may injure the lung; however, the relative importance of intracellular versus extracellular free radicals is unclear. The superoxide dismutases (SOD) are the primary enzymatic method to reduce
Resuscitation with macromolecular superoxide dismutase/catalase mimetic polynitroxylated PEGylated hemoglobin offers neuroprotection in guinea pigs after traumatic brain injury combined with hemorrhage shock.
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Serum malondialdehyde, erythrocyte glutathione peroxidase, and erythrocyte superoxide dismutase levels in women with early spontaneous abortions accompanied by vaginal bleeding.
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BACKGROUND
Malondialdehyde (MDA) is a marker of lipid peroxidation. Glutathione peroxidase (GPX) and superoxide dismutase (SOD) are the main enzymes responsible for the detoxification of superoxide anion. The aim was to assess whether serum MDA, erythrocyte GPX, and erythrocyte SOD levels altered
Evidence for extracellular superoxide dismutase as a mediator of hemorrhage-induced lung injury.
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Hemorrhage results in excessive production of superoxide that is associated with severe lung injury. We examined whether the superoxide dismutase (SOD) mimetic manganese(III) mesotetrakis (di-N-ethylimidazole) porphyrin (AEOL 10150) could attenuate this lung injury and whether extracellular
Superoxide dismutase activity in cisternal cerebrospinal fluid after aneurysmal subarachnoid haemorrhage.
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It has been recognised that the level of superoxide dismutase (SOD) significantly increases in CSF as the result of cerebral ischaemic damage. The aim of this study was to correlate the CSF levels of SOD enzymatic activity to the patterns of subarachnoid haemorrhage with regards to ischaemic
Superoxide dismutase and allopurinol improve survival in an animal model of hemorrhagic shock.
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We studied the efficacy of resuscitation with antioxidants in an animal model of hemorrhagic shock. Male Sprague-Dawley rats were anesthetized, and 27 mL/kg of blood was withdrawn from the carotid artery over 2 minutes. The animals remained in hemorrhagic shock for 45 minutes, followed by 1 hour of
Pentoxifylline alone versus pentoxifylline combined with superoxide dismutase prolongs survival in a rat hemorrhagic shock model.
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Pentoxifylline (PTX) and superoxide dismutase (SOD) have each proven effective in improving survival when administered during resuscitation in animal models of hemorrhagic shock. This study was conducted to determine if PTX and SOD combined would have synergistic effectiveness in the treatment of
Amelioration of vasospasm after subarachnoid hemorrhage in transgenic mice overexpressing CuZn-superoxide dismutase.
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OBJECTIVE
To clarify the effect of superoxide dismutase (SOD) on vasospasm after subarachnoid hemorrhage (SAH), we investigated sequential changes in arterial diameter after SAH in transgenic mice overexpressing CuZn-SOD (SOD-1).
METHODS
SOD-transgenic mice and nontransgenic littermates (35 to 40 g)
Transgenic CuZn-superoxide dismutase inhibits NO synthase induction in experimental subarachnoid hemorrhage.
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OBJECTIVE
The expression of inducible NO synthase (iNOS) after experimental subarachnoid hemorrhage (SAH) has been postulated to play a critical role in the pathogenesis of SAH and subsequent cerebral vasospasm. The inhibitory effect of CuZn-superoxide dismutase (CuZn-SOD) on the induction of iNOS
Effects of cyproheptadine on plasma superoxide dismutase activity and malondialdehyde content in rabbits with hemorrhagic shock.
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Profound hemorrhagic shock was produced in thirty rabbits by exsanguination via the carotid artery until blood pressure (BP) reached 5.3 kPa (40 mmHg) and was sustained for a period of 90 minutes. The rabbits were equally divided into cyproheptadine (Cyp) treated group and control group. Blood
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