| Objective: Intracerebral hemorrhage (ICH) is a severe disease to endanger the people's life because of its high incidence rate, fatality rate and serious disability. There is no effective therapy in clinical work. The pathogenesis and pathophysiology of ICH are very complicated. So there is lots of research about it. Most researchers believe that the secondary injury surrounding the hematoma is the main cause which leads to the deterioration of nerve function. The most important pathophysiological change is the secondary brain edema following ICH. The reason of brain edema formation is very complicated. Hemoglobin release after erythrocyte cytolysis in the hematoma and inflammatory cytokine participation may be important reasons in the brain edema formation after ICH. It has been found by experimental and clinical research that the activation of complement played an important role in inflammatory response of ICH. The activation of complement is very important in protecting body, controlling infection and plerosising the injury tissue. But over activation of complement or not appropriate immune reaction will do harm to the host. The complement cascade activation following ICH has advantageous to accelerating erthrocyte cytolysis and it can damage the parenchyma cells. Our study is to investigate the activation and effects of complements in brain edema formation after ICH. Methods: In this study, 66 pentobarbital-anesthetized Sprague-Dawley rats were used. A cranial burr hole (1.0 mm) in the skull (1 mm anterior, 4.0 mm right to the bregma) was drilled, then 50μl autologous caudate artery blood was infused into right caudate nucleus of the rats stereotacticaly. Sham rats underwent intracranial needle placement without blood infusion. The rat's behavior was evaluated at 6, 12, 24, 48, 72 hours and 7 days after operation and the scores were recorded. The rat's behavior was evaluated by 4 methods, including Longa Score, Footfault Asymmetry Score, Berderson Score and Balance Beam Score. Then rats were decapitated and the intact brain was taken out. The brain was cut from the hole coronally. The hematoma can be seen in the right caudate nucleus. The brain was cut into 4 mm thick. Brain water content was tested by dry-wet weigh method. The pathological changes including hematoma, brain edema and inflammatory cells infiltration in surrounding hematoma or within the clot were observed by HE staining. Complement 3 expression in rat brain at different time was investigated by immunohistochemistory. Results: ①The left limbs of rats was hemiplegia after operation. The behavior changes were no difference betweenthe ICH group and the sham group at 6 h after operation. Possibly the anesthetic and operation injury lead to the result. The behavior changes score increased at 12 h, peaked at 48 h, decreased at 72 h and recovered normal at 7 d. This suggested corresponding behavior was consistented with brain damage. ②Brain water content had no difference at 6 h between ICH group and sham group (77.99±0.112% versus 77.69±0.384%). But it elevated at 12 h (78.13±0.518%),peaked at 48 h (79.49±0.251%)--72 h (78.47±0.272%), decreased at 7 d (78.12±0.453%) in ICH group. In 48 h group and 72 h group, brain water content was significant different between the ICH group and the sham group. In ICH group, brain water content of 48 h and 72 h was significant different from other time points. ③There were few inflammatory cells infiltration in the brain of sham group and contralatera of ICH group. Inflammatory cells became apparent in perihematoma at 12 h and 24 h, and were more abundant at 48 h, then decreased gradually till disappearing at 7 d. ④There were a few complement positive cells in both sides of sham group. Compared with the contralatera, the expression of C3 in ipsilateral increased at 6 h (17.29±4.38) and reached maximum at 72 h (83.60±11.30) after blood injection, and decreased until 7 d. In the clot there was no positive cell at 6 h after ICH, but many C3 positive neutrophils was found at 48 h. Then the positive neutrophil... |
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