The Effect of Hyperbaric Oxygen on Brain Macrophage after the Postischemic Stroke in Rats
碩士 === 國防醫學院 === 生物及解剖學研究所 === 90 === Cerebral hypoxia is a major component of immediate and secondary cell damage caused by ischemia.The optimal clinical management of cerebral ischemic insult to the brain remains problematic.Various therapeutic regimens including hyperbaric oxygen have...
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| Format: | Others |
| Language: | zh-TW |
| Published: |
2002
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| Online Access: | http://ndltd.ncl.edu.tw/handle/27688029976513797732 |
| Summary: | 碩士 === 國防醫學院 === 生物及解剖學研究所 === 90 === Cerebral hypoxia is a major component of immediate and secondary cell damage caused by ischemia.The optimal clinical management of cerebral ischemic insult to the brain remains problematic.Various therapeutic regimens including hyperbaric oxygen have been proposed to protect the brain after an ischemic insult. Recent evidence showed the HBO treatment can reduce cerebral infarction area and decrease neurological deficits. Also recent evidence suggests that glial cells play an active role in the importance of active neuronal-glia interaction in the maintenance of homeostasis. These function become more significant in respose to a CNS insult such as ischemia. Observations on early reactions of microglia and macrophage after brain injury will be essential to clarify the contributions of these two cell types to the brain’s response to injury. A rat model of reversible occlusion of the middle cerebral artery (MCAO) was developed to assess the relationship of cellular elements and prophylactic hyperbaric oxygen on cerebral injury. Now we have investigated the reaction of brain macrophage after MCAO with/without HBO. The responses of brain macrophages were also exammined with antibodies, OX42, OX6 and ED1. Our results showed that HBO treatment reduced the population of brain macrophages bearing CR3 receptors (OX42) in the infarction area, but not those of brain macrophags with MHC class II antigen (OX6) or macrophage lysosomal protein (ED1). The marked attenuation of OX42 labeled brain macrophages indicated an effective suppression of monocytic invasion in the lesioned cortex. These results may provide the possible mechanism of early HBO therapy in the postischemic stroke of rats on glia reactions.
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