| Summary: | 碩士 === 高雄醫學大學 === 醫學研究所碩士班 === 93 === Abstract
Systemic sepsis and its consequences are the commonest causes of death in intensive care units. Systemic sepsis frquenttly produces brain dysfunction or sepsis-associated encephalopathy (SAE) which is an early sign and may occur in up to 70% of patients. However, the mechanism is still under investigation. In our previous study, we showed that heat shock (HS) pretreatment reduced mortality in septic rats, and protected the cortical function in hypoxia or drug-induced convulsion. In this study, it was designed to investigate whether the HS plays the protective role in SAE and its possible mechanism was discussed. Male Spraque-Dawley rats were used as the experimental animal and SAE was induced by intraperitoneal injection of Lipopolysaccharide (LPS;7.5,15&30 mg/kg) . Electroencephalography (EEG) was used to evaluate the cortical function. Western blot analysis was used for evaluating the iNOS, Arc and heat shock protein (Hsp) 72. The results showed : (1) The background activity of EEG got slow down 10 minutes after LPS administration in both groups, while those of the heated group was significantly attenuated. (2) Spiky activities were found more abundantly and earlier in non-heated septic rats. (3) LPS (7.5mg/kg)-injected group showed iNOS expression in the brainstem but reduced in the heated LPS-injected group. The amount of Arc, one of immediate early genes, was decreased both in the cortex and hippocampus of LPS (30mg/kg)-injected group. We concluded that LPS injection decreased the cortical electric activity while it could be attenuated by pretreatment of heat shock. Increased synthesis of iNOS in the brainstem and decrease in Arc expression in cortex might participate in the pathogenesis of SAE.
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