| [Background] thrombolysis therapy in the early initiatory time of thrombosis isregarded as the effective method in the treatment of acute cerebral infarction. Butthere are still three major problems remain unsolved well: 1) reocclusion; 2)reperfusion injury;3) secondary haemorrhage.[Objective] This study observe the safety of Batroxobin after usingUrokinase to prevent reocclusion in the rabbit with acute cerebral infarction atdifferent time.[Method] 30 male healthy New Zealand rabbits were randomizedly divided into fivegroups:1) normal control; 2) model control;3) group 1 of therapy;4) group 2 of therapy;5) group 3 of therapy. Each groups contains 6 animals. The rabbit model wereestablished by using self embolism to embolize the cerebral artery throughintracervical artery. Rabbits in group 1 of therapy were transfused with 40,000U/kg ofUrokinase 2 hours after model formation through vein; Group 2 were infused with thesame dosage of Urokinase plus 2.5BU/kg of Batroxobin; Group 3 were firsttransfused with Urokinase, then transfused with the same dosage of Batroxobin 3hours later; while normal control and model control were infused with normal salineat the same dosage. Activated partial thromboplastin time(APTT), prothrombin time(PT), fibrinogen(FIB) and thrombin time(TT) were measured in every group withThrombosaeen400C grumemeter at different time: before model forming; 2hr aftermodel formation; 6hr after treatment; 22hr after treatment. Platelet adhesion reactionrate(PAR) were measured with 3-9D syntheticmeter. The brain tissues were obtained through head cutting 22hrs after treatment, frozen section were used toobserve if there were cerebral hemorrhage, 2％tetrazolium (TTC)dyeing to observe ifthere were infarction focus at brain. Brain tissue were fixedwith 10％formalin. Thehistopathological changes of the brain tissue were observed by light microscope afternormal paraffin section, HE dyeing. At the same time, the centra area of the infarctionside of the brain tissue were cut out to made the tissue homogenate. The activity ofsuperoxide dismutase(SOD) were measured by pyrogallic acid autoxidation method.The content of MDA were measured by thiobarbitaiacid method.[Results] There are no significant difference in various index among each groupbefore cerebral infarction (p＞0.05). The results of corresponding period after cerebralinfarction are shown below:1. the change in histomorphology of cerebral infarction after thrombolysis treatment:There were no brain hemorrhage both in normal control and model control,There were 2 cases of brain hemorrhage both in group 1 and group 2, There were 1cases of brain hemorrhage in group 3. There are no significant difference amongeach group. 6 normal control rabbits were all normal by the TTC dyeing, but foundinfarction focus on all 6 model cases. There were no significant difference amongeach of 3 therapy groups on TTC dyeing(p＞0.05): group 1 (2 cases normal,2 caseshad focus); group 2 (2 cases normal, 1 case had focus); and group 3 (3 cases normal, 2cases had focus).2. The change of FIB, PT, APTT, TT on cerebral infarction's rabbits by thrombolysistreatment:Compare with before modeling, The changes of FIB, PT, APTT, TT in normalcontrol group had had no statistical value(p＞0.05). Compare with before modelingor same period (normal control group), the FIB in model control group had increasesignificantly, and the PT, APTT, TT had decrease down After mode-ling,, both havestatistical value(p＜0.05). Compare with 2 hours after modeling or the same period of model group,the FIB in group 1,2,3 had decrease down obviously at 6 hours aftertreatment, while the PT, APTT, TT has increase remarkably (p＜0.05). Comparewith the same period of model group,the FIB in group 1,2,3 had decrease down at 6hours after treatment, while the PT has increase remarkably (p＜0.05). Comparewith group 1 at 6hrs after treatment,the FIB, PT, APTT in group 2,3 had changedadvancely at the same tendency(p＜0.05), while there were no difference betweengroup 2 and group 3 in every index at every period.3. The influence of thrombolysis treatment to the PAR:The PAR had no difference between every spot in normal control. The PAR ofmodel group increased markedly after modeling.compare with before model formingor normal control, the PAR of model group had increased markedly(p＜0.05), the PARof all three therapiiag groups were increased remarkably at 2hrs after modelingcompare with before (p＜0.05), but it decreased obviously at 6hrs after treatment. Thevalue of PAR in all three theraping groups at 6hrs after treatment were decreasedmarkedly than the model group at the same period(p＜0.05). The PAR of group2 andgroup 3 were decreased markedly at 6hrs after treament than group 1 (p＜0.05), whilethere were no difference between group 2 and group 3 at every period.4. The influence of the content of SOD and MDA by thrombolysis treatment incerebral infarction:The content of SOD were the highest in nomaal control, and the loewest inmodel control among all five groups. The SOD of group 1 increased markedly thanmodel group(p＜0.05). The SOD in group 2 and 3 increased markedly Compare withgroup 1 (p＜0.05), while there were no difference between group 2 and group 3. Thecontent of MDA of all three theraping groups were lower than the modelgroup(p＜0.05), while there were no difference among 3 theraping groups.[Conclusion] Through pathobiological observation, the result of this studyshow that Batroxobin are safe at a range of dosage in the treatment of acute cerebral infarction after using Urokinase in rabbits. After Urokinase injection, Batroxobincan diminish the reperfusion injury, but didn't increase the incidence ofhaemorrhage. The four index of blood coagulation show that blood coagulationfunction drop markedly through the combinative therapy with urokinase andBatroxobin. In order to decrease incidence of haemorrhage, we must control thedosage strictly and supervise coagulation-fibrinolytic function.
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