ray ban sunglasses Lipid peroxidation in cerebral

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Lipid peroxidation in cerebral ischemia reperfusion injury induced flow

Quality content in Table 1,[link widoczny dla zalogowanych], Table 2,[link widoczny dla zalogowanych], Table 3.2 Yumin lipid peroxidation in cerebral ischemia reperfusion injury 4l flow compared with control group,[link widoczny dla zalogowanych], p <O05,} p <O. 01; compared with the ischemia group, ap <O. 05, bp <O. 0l perverse effects from Table 2 ± SD) skin repeatedly brain Na +, K (mEq/kg-T- 'l'), H2o ink ca Gan (swollen 0l / g Nirvana weight) were compared with the HC group, a P <001 Table 3 super chloride dismutase on ischemic reperfusion flow of the skin after repeated brain Na, K a (mlgq / kg dry weight) content of the summer slow H20 ± SD) and I-R group, P <0.05, Kunming Medical Hospital volume of the first l0 2'3 cortex Tx ,6-keto-PGFn content shown in Table 4. Table 4 hyperoxia on the cerebral cortex after ischemia and reperfusion flow TxB2 ,6 - keto-PGF1 amount of buildings ± SD) and C, I group, P <005, a P <001: Compared with I , + P <0.05. The number in parentheses is the number of animals 2'4 cortex malondialdehyde (MDA) content in Table 5. Table 5 high concentration of oxygen flow to the brain after ischemia and reperfusion repeated MDA content of the skin ± SD) compared with other groups, a P <0012'5 electron microscope observation of morphological changes of nerve cells in ischemia 60 minutes, see the nerve cellular edema, mitochondrial swelling, cristae rupture, dissolve, disappear. High concentrations of air or oxygen environment after reperfusion flow, these changes increase, and the emergence of rough endoplasmic reticulum degranulation, and calcium deposition in mitochondria of ischemic necrosis of nerve cells and other serious pathological changes. 3 discuss the above results show that the experiment successfully replicated the flow cerebral ischemia reperfusion syndrome model of ischemia reperfusion flow after the performance, EEG severe depression, brain water, sodium, calcium increase, TXB, increased 6 a keto -PGFI2 decrease in lipid peroxidation was significantly increased in high-oxygen environment, morphological examination revealed further aggravate ischemic neuronal damage for ischemic reperfusion injury in the pathogenesis of flow, from the lipid peroxidation and prostaglandin metabolism, water and electrolyte metabolism, the relationship between high concentrations of oxygen, etc. were discussed. In the process of prostaglandin metabolism (PGG, converted to PGH, ,5-HPETE into UrS) free radicals, the formation of lipid peroxides. Lipid peroxides and thus enhance the degradation of the membrane phospholipids, promoting prostaglandin metabolism cascade, leading to and increased TXA, and PGI2 imbalance, to form of prostaglandin metabolism and lipid peroxidation in the circulation pathway. Of their own design with the first high-oxygen environment of a high concentration of oxygen on cerebral ischemia reperfusion flow of brain lipid peroxide malondialdehyde metabolic end product of a (MDA), the impact of two Yumin lipid peroxidation in the sand flow of cerebral ischemia reperfusion injury 43 ring. The results showed that high concentrations of oxygen can significantly increase the flow of ischemic reperfusion formation of MDA in brain tissue, but the water, electrolyte, there is no corresponding prostaglandins and morphological changes. That lipid peroxidation precedes membrane damage. So when the treatment is not appropriate, you can further lead to cell death. Accordingly, the authors suggest that high concentrations of high-pressure oxygen therapy has a strict adaptation levy, its efficacy depends on the severity of cerebral ischemia time and oxygen. When early ischemic inhalation of high oxygen, because oxygen supply to increase ischemic tissue, ischemic tissue may maintain normal energy metabolism, so that the damage reduced. And severe ischemia reperfusion flow, due to mitochondrial damage, energy supply and demand imbalance, thus giving high concentrations of oxygen can enhance the lipid peroxidation and increased tissue damage. SOD significantly reduced ischemia reperfusion flow of water in brain tissue sodium content, and water for 60 minutes with ischemia no significant change in sodium content. The results showed that after reperfusion flow of free radicals, lipid peroxides, lipid peroxides and thus increase the water and electrolyte metabolism imbalance. In the high concentration of oxygen after ischemia to reperfusion flow environments found no ca, Na, H, O content increased in parallel with the MDA, its mechanisms remain to be further investigated. Membrane lipid peroxidation can DNA strand breaks and protein cross-linking reaction occurs, biofilm injury. Electron microscope found that calcium deposition in mitochondria, nerve cells appeared irreversible change. The above analysis shows that after ischemia and reperfusion flow membrane lipid peroxidation may be involved in multiple pathological metabolic processes and lead to severe nerve cell damage. Thus, membrane stabilizer free radical scavenger to reduce free radicals after ischemia and reperfusion flow, formation of lipid peroxide, on cerebral ischemia reperfusion injury in flow will play an important role.

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