| Background：Fluoroacetamide is a kind of highly toxic rodenticide of organicfluorine type, and has strong neurovirulence to both people and livestock.Its recognized mechanism of action is that, fluoroacetamide turns intofluorine citric acid under the enzymatic function after it enters into theorganism, blocks the tricarboxylic acid cycle and results in energymetabolic disturbance of the cells. Acetamide is an effective antidote, andbecause of its similar chemical construction with fluoroacetamide, acompetitive mechanism can be formed between them to reduce theproduction of poisonous products. However, serious fluoroacetamideintoxicated patients will die in very short time, because it can causeserious damage to the organism, especially to the brain. Therefore,studying the effective therapeutic methods after fluoroacetamidepoisoning is of important significance to the reducing of case fatality rateand improvement of clinical prognosis.Objective：To discuss and study the therapeutical effects of different medicinesafter fluoroacetamide poisoning, and observe the protective effects ofulinastatin to brains in the therapeutic process of fluoroacetamidepoisoning.Method：Model of healthy rats for study of fluoroacetamide poisoning wasprepared through the gavage method, and they were divided into A, B, C and groups in random. Group A was the normal control group; rats in thisgroup were given1ml of normal saline by gavage and then given normalsaline everyday by intraperitoneal injection. Group B wasfluoroacetamide contamination group; rats in this group were givenfluoroacetamide solution with the concentration of6mg/kg by gavage toproduce a fluoroacetamide poisoning model, and they were given isodosenormal saline by intraperitoneal injection everyday. Group C wasacetamide treatment group; rats in this group were given fluoroacetamidesolution with the concentration of6mg/kg by gavage to produce afluoroacetamide poisoning model; after contamination, they were givenacetamide1hour later for the first time (2.8g/kg, intraperitoneal injection)and12hours later for the second time (2.8g/kg, intraperitoneal injection).Group D was acetamide+ulinastatin group; rats in this group were givenfluoroacetamide solution with the concentration of6mg/kg by gavage toproduce a fluoroacetamide poisoning model; after contamination, theywere given acetamide1hour later for the first time (2.8g/kg,intraperitoneal injection) and the same dosage12hours later for thesecond time, but they were given ulinastatin every time additionally(55000iu/k, twice a day, intraperitoneal injection). After contamination ofhealthy rats, the HE staining of their brain tissues were collected atdifferent times (4h,1d,3d,7d) to observe the morphological changes ofthe brains and the expressions in the tissues combined withimmunohistochemistry method, and the GABA and Glu of hippocampusin the brains were observed; the dynamics of immunoreaction wereshowed in gray values, then statistical analysis was carried out to discussits significance.Results：By immumohistochemical staining to the GABA and Glu and measurement to the gray values, statistical results show that after thepoisoning of rats, the GABA and Glu expressions will increase. TheGABA and Glu expressions of Group D (Ulinastatin Group) increasedcompared to Group A (Control Group), and are weaker than those ofGroup B (Contamination Group) and Group C (Acetamide Group). TheHE staining of all groups at4h,1d,3d,7d have no pathologic changes.Conclusion：Fluoroacetamide poisoning will cause damages to brain tissues ofrats, and GABA and Glu expressions play an important role in braindamage after fluoroacetamide poisoning. Ulinastatin injection cansignificantly restrain the GABA and Glu expressions, and have obvioustherapeutic effects to the brain tissues after fluoroacetamide poisoning. |
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