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Objective To study the correlation between the coagulation factor Ⅶ (F Ⅶ) and progressive hemorrhage after brain contusion in mice and provide the experimental evidence for the clinical application of recombinant human FⅦa.Methods Twelve male BALB/c mice were given liposomeencapsulated FⅦsiRNA via tail vein at doses of 1,3,5 and 10 mg/kg with 3 mice per dosage.The other 3 mice received equivalent volume of normal saline as controls.Two days after the injection,mice blood sampling was used to detect FⅦ mRNA expression in liver using real-time PCR,level of plasma FⅦ using ELISA method,and activity of plasma FⅦ using chromogenic substrate assay.The optimal dose at which F Ⅶ expression was inhibited was determined.Thirty BALB/c male mice were assigned to two groups (n =15 per group) according to the random number table:FⅦ-suppressing group,mice were injected with FⅦsiRNA at the optimal dose and control group,mice were injected with same volume of negative control vector.The model of brain contusion was established in both groups.Volume of hemorrhage following brain contusion was measured at 3,24 and 72 h postinjury,and hematoma volume at 24 and 48 h postinjury.Results Liposome-encapsulated siRNA delivery down-regulated FⅦ expression in the mouse liver.Level and activity of plasma FⅦ were also reduced significantly.The optimal siRNA dose was 3 mg/kg.At 3,24 and 72 h postinjury,relative volume of brain hemorrhage in FⅦ-suppressing group was 1.46 ± 0.10,1.82 ± 0.23 and 2.28 ± 0.15 respectively,significantly higher than that in control group (1.00 ± 0.25,1.20 ± 0.31 and 1.20 ± 0.22 respectively) (P ＜ 0.05).At 24 and 48 h postinju-ry,volume of hematoma in FⅦ-suppressing group was (6.7 ± 1.5)mm3 and (9.8 ± 1.0) mm3,significantly higher than that in control group [(5.2 ± 1.2) mm3 and (5.5 ± 1.5) mm3] (P ＜0.01).Conclusions Level of FⅦ in vivo relates closely to the progressive hemorrhage of brain contusion in mice.Administration of FⅦ is effective to reduce the incidence of progressive hemorrhage.
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Objective To investigate the technique of transarterial embolization of dural carotidcavernous fistulas(DCCFs)with low concentration(14%-25%)of n-butyl-cyanoacrylate(NBCA)and determine its value.Methods Eight patients with DCCFs were treated by transarterial embolization with low concentration of NBCA using a wedged microcatheter.Of the 8 patients,5 had unsuccessful transvenous embolization and 3 could not be treated with transvenous embolization.Results Transarterial embolization with low concentration of NBCA using a wedged microcatheter resulted in complete obliteration of the affected cavernous sinus and related shunts in 5 patients,no residual arteriovenous shunt was demonstrated on postembolization angiography.On clinical and angiographic follow-up 6-12 months later,complete resolution of clinical symptoms was observed in all 5 patients and there were no recurrent or residual DCCFs found.Partial obliteration of the involved cavernous sinus and the related shunt was achieved in the remaining 3 patients on immediate post-procedure angiography,but the volume of shunt diminished significantly.On clinical and angiographic follow-up 3 months later,in 2 patients,clinical symptoms were improved and the arteriovenous shunts were diminished;in the third patient,clinical symptom resolved and the shunt was obliterated.There were no major complications except for the transient worsening of ocular symptoms due to Ⅵ cranial nerve palsy in 1 patient.Conclusions Transarterial embolization of DCCFs with low concentration of NBCA using a wedged microcatheter was a safe and effective treatment method.It is an optimal alternative for the patients with DCCFs in which transvenous route was unsuccessful,or impossible.
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Objective To investigate endovascular treatment of traumatic direct carotid-cavernous fistulas (CCF) and their complications such as pseudoaneurysms. Methods: Over a five-year period, 22 patients with traumatic direct CCFs were treated endovascularly in our institution. Thirteen patients were treated once with the result of CCF occluded, 8 twice and 1 three times. Treatment modalities included balloon occlusion of the CCF, sacrifice of the ipsilateral internal carotid artery with detachable balloon, coil embolization of the cavernous sinus and secondary pseudoaneurysms, and covered-stent management of the pseudoaneurysms. Results All the direct CCFs were successfully managed endovascularly. Four patients developed a pseudoaneurysm after the occlusion of the CCF with an incidence of pseudoaneurysm formation of 18.2% (4/22). A total number of 8 patients experienced permanent occlusion of the ICA with a rate of ICA occlusion reaching 36.4% (8/22). Followed up through telephone consultation from 6 months to 5 years, all did well with no recurrence of CCF symptoms and signs. Conclusion Traumatic direct CCFs can be successfully managed with endovascular means. The pseudoaneurysms secondary to the occlusion of the CCFs can be occluded with stent-assisted coiling and implantation of covered stents.
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Objective To investigate the clinical, radiological features and therapy of spinal actinomycotic infection complicated with spinal cord compression.Methods The data of three patients confirmed by histopathology were analyzed retrospectively.Results All three patients presented with infection of cervical thoracal vertebral bodies and soft tissue, and with syndrome of spinal cord compression. MRI examination revealed destruction of vertebral bodies, extradural soft tissue mass and spinal cord compression. Histopathological examination confirmed the infection of actinomycete in all three patients. Granulomatous inflammation could be seen in two cases, while extradural abscess was found in the other one case. Three patients all received the operation of abscess draining and vertebral canal decompression. Large-dose of Penicillin G following operation was administrated intravenously for 4～8 weeks, and then changed to oral application for another 4～6 months. Follow-up showed significant clinical effect in these three patients.Conclusions Radiologic and clinical findings of spinal actinomycotic infection complicated with spinal cord compression are nonspecific, and the diagnosis of this disease depends on pathological and microbiologic exams. Treatments with abscess draining, vertebral canal decompression and large-dose of antibiotic may achieve good clinical outcome.