| Cerebral hemorrhage is a very common clinical disease with high mortality and morbidity rate, however, both many animal experiments and clinical studies found that little even middle level hemorrhage itself did not increase the intracranial pressure, thus, the tissue edema around the hemorrhage and secondary neuron injuries may be one of the reasons for the severe sequence. Due to the uncertainty of the real mechanism of the occurrence and progress of the disease, the effective treatment is by far not available. The possible mechanism of the cerebral edema secondary to .cerebral hemorrhage within reach till now may be summarized as follows: the tissue rschemia and anoxia around the hemorrhage; the action of the thrombin;the effect of component of the hematoma; immune and inflammatory reaction. The role of the immune inflammatory reaction on the brain injury has been gradually paid attention to in recent years and many literatures confirm that brain injury may generate and activate the inflammatory cells which can release plenty of inflammatory cytokines such as TNF-α , IL-8, IL-6 etc. belonging to the medium of complement protein families. As we all know, complement system is the important component of the inflammatory reaction and humoral immunity which stands immune defence and immunoloregulation and may mediate the immunopathological destructive reaction. In recent years many domestic and foreign experimental and clinical data both manifest that complement system plays an important role in the inflammatory reaction after brain injury. The study of Davis et al found that the C4 level decreased in the cerebral infarction patients while the level of membrane attack complex (MAC) was obviously higher than that of. the normal in 1992 and the research of Lindsberg et al on the complement activation of the human blood brain barrier and central nervous system also verified that there was different level of C9 deposition in the cerebral infraction area and the surrounding edema zone in human brain tissue in 1998. Guohuaxi' s study also found the extent of cerebral edema declined and inflammatory infiltrationreduced when cerebral hemorrhage occurred in the complement system exhausted rat model and the result induced that the complement system may contribute to reducing the hemorrhagic cerebral edema to some extent.The cobra venom factor(CVF) is a nonvenomous glycoprotein extracted from the cobra venom which can split C3 and C5 activated by the alternative complement pathway. The CVF can activate the complement and exhaust it at last as well and is an ideal tool to study the complement. All the data available on the study of the relationship of the complement system and nervous system is rare and the related research are all confined to the study of the normal animal after complement system exhausted, such as the relationship between the complement system exhausted and cerebral infarction, the study of complement system exhausted in a large area burned rat etc. while the report of the effect of excessive activation of the complement system on cerebral edema is few. This experiment is toobserve the change of the water content in the brain tissue after acute cerebral hemorrhage and the variation of the concentration of Tumor necrosis factor (TNF-α) and Neuron-specific enolase (NSE) in different observation time by activating the complement system through CVF in rabbits and study the dynamic changes of the complementsystem on the cerebral edema after cerebral hemorrhage and the concentration of the TNF and NSE so as to find a practicable way to treat the hemorrhagic cerebral edema.Materials and Methods1.1 Material and experimental groupsA total of 56 male Japanese White rabbits (weight, 2300 + 300 g) were provided with animal-experiment center of Wenzhou Medical College. The experiments were divided into 4 groups, consisted of a control group, a CVF-treated group, a vacuity group and a standard group.1.2 Experimental procedures and MethodsJapanese White rabbit'...
|
PDF Full Text Request