superoxide dismutase/hemorrhage

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

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

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 Following instrumentation and stabilization, blood was withdrawn to reduce mean arterial pressure to 35 mmHg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 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

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

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

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

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

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

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 (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

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)

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

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