ABSTRACT
Objective To study the efficacy of complement depletion with CVF in preventing a-cute rejection after heart allotransplantation in inbred strain rats. Methods Inbred male Lewis rats were used as recipients and Brown-Norway rats as donors, and the heterotopic heart transplantation model was established. The allografts were divided into 2 groups (n=8 in each group). After infusing low-dose CVF 20?g/kg to the CVF-treated group, cardiac allograft survival time was observed on 4 rats of each group. The remaining 4 rats in each group were killed respectively at day 1,3,5 and 6, the pathological grade for acute rejection, the complement activity in serum, the deposition of C3 on tissue, and the extent of infiltration by CD3+ T cells were compared. Results The mean survival time of heart allograft was (11. 69?0. 72) days and (6. 65?0. 35) days in CVF-treated group and control group respectively (P
ABSTRACT
AIM To establish the model of exudative pleurisy induced by alternatively activating complement and to study protection of anti inflammatory drugs on it. METHODS Purified cobra venom factor (CVF) was injected into the pleura, and then exudate volumn, total leukocyte count, protein content and histamine concentration were determined. RESULTS CVF, injected into rat pleura at dose of 0 08～2 mg?kg -1 , induced exudative inflammation in dose dependent and time dependent manner. Both diphehydramine and isoprenaline reduced significantly exudate volume, total leukocyte count, protein content and histamine concentration, while indomethacin, dexamethasone and cyclophosphamide also reduced exudate volume, total leukocyte count and protein content, although they did change the release of histamine. DLF, one of the toxic components in cobra venom, potentiated CVF induced inflammation. CONCLUSION CVF can induce significantly exudative pleurisy sensitive to anti inflammatory agents. DLF has augmentation on CVF induced inflammation.