The pre-treatment effect on brain injury during restoration of normal perfusion pressure with hemodilution in a new rat model of chronic cerebral hypoperfusion.

OBJECTIVES: To investigate the effect of hemodilution with high-concentration human serum albumin (HSA) on brain injury in a rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations. METHODS: The animal model was established by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein and the ipsilateral common carotid artery, followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. The agent (20% HSA) or control solution (0.9% sodium chloride) was administered intravenously at a dosage of 1% body weight 24 hours before ligation of the fistula. Blood-brain barrier (BBB) disruption was judged by extravasation of Evans blue (EB) dye. EB, water content and the changes of myeloperoxidase (MPO) activity and superoxide dismutase (SOD) activity in rat brains 24 hours after ligation of the fistula were determined. RESULTS: EB and water content in rat brains of the pre-treated group were significantly decreased compared with the control group accompanied by reduction of MPO activity and enhancement of SOD activity. DISCUSSION: Hemodilution with high-concentration HSA has a certain pre-treatment effect on brain injury after ligation of the fistula in rat model of chronic cerebral hypoperfusion, which may be resulted from improved microcirculation, decrease in inflammatory cell infiltration and inactivation of oxygen free radicals.

[Treatment and prevention of cerebrospinal fluid leakage after craniofacial surgery for tumors involving the skull base].

PURPOSE: To evaluate the treatment and prevention of cerebrospinal fluid (CSF) leakage following removal of the skull base tumors with craniofacial approach. METHODS: A retrospective review was undertaken to analyze the clinical data of 14 cases suffering from CSF leakage after craniofacial surgery for tumors involving the cranial base. RESULTS: Ten (71.4%) case cured between 3 days and 32 days by conservative treatment including lumbar drainage. Three of four patients who needed operation had no CSF leakage after first attempt. One discontinuous leakage was closed after a second attempt. Among all cases,five(35.7%) patients developed meningitis,and one case died because of serious intracranial infection and respiration failure. CONCLUSION: Continuous lumbar cerebrospinal fluid drainage is a safe and effective treatment of CSF leakage following craniofacial surgery. However,If conservative treatment fails to arrest CSF leakage,surgical therapy is recommend with multilayer reconstruction for dural defect so as to avoid meningitis. The vital procedure for prevention of CSF leakage is watertight seal of dura mater, reconstruction of bone defect and obliteration of dead space after craniofacial surgery.

Vascular endothelial growth factor expression and angiogenesis induced by chronic cerebral hypoperfusion in rat brain.

OBJECTIVE: In a rat model, we studied the time courses of vascular endothelial growth factor (VEGF) expression and angiogenesis induced by chronic cerebral hypoperfusion in the brain, and we investigated the histological basis of normal-perfusion pressure breakthrough. METHODS: Twenty-one Sprague-Dawley rats were randomly divided into a control group (n = 3) and a model group assessed at various time points after the creation of a carotid artery-jugular vein fistula (12 h, n = 3; 24 h, n = 3; 72 h, n = 3; 7 d, n = 3; 21 d, n = 3; 90 d, n = 3). The time courses of the expression of VEGF messenger ribonucleic acid (mRNA) and protein in rat brain were analyzed with semiquantitative reverse transcriptase-polymerase chain reaction and Western blot assays, respectively. Immunohistochemical techniques were used to evaluate VEGF protein localization with rabbit polyclonal anti-rat VEGF, VEGF receptor (VEGFR) expression with rabbit polyclonal antibodies to VEGFR-1 and -2, microvascular density with mouse monoclonal anti-rat CD31, and astrocytic reactivity with polyclonal anti-glial fibrillary acidic protein, in cerebral cortical tissue of the right middle cerebral artery territory. RESULTS: Three alternative splicing forms, i.e., VEGF(188), VEGF(164), and VEGF(120), were observed in cerebral cortical tissue of the right middle cerebral artery territory in semiquantitative reverse transcriptase-polymerase chain reaction analyses. VEGF(164) mRNA was the predominant isoform expressed in rat brain. VEGF(188) mRNA and VEGF(120) mRNA were also detected but at very low levels (not statistically significant). Low levels of VEGF(164) mRNA were observed in the control brains. However, VEGF(164) mRNA levels were significantly increased in the model brains at 24 hours postoperatively, peaked by 7 days, decreased by 21 days, and returned to basal levels by 90 days after fistula formation. VEGF protein expression, as measured in Western blot assays, was also increased in rat brains in the model group from 24 hours to 21 days postoperatively but returned to control levels by 90 days after fistula formation. VEGF immunohistochemical analyses indicated that this increased expression was mostly associated with endothelial cells. Consistent with the VEGF protein expression findings, up-regulation of VEGFR-1 but not VEGFR-2 expression on endothelial cells in the model brains was observed. Microvascular density in the rat brains began to increase significantly 7 days after fistula formation in the model group, as assessed immunohistochemically, and the increase was maintained for 90 days. Although no prominent astrocytic reactivity was observed in the rat brains throughout the experiments, there was an absence of astrocytic foot processes surrounding some cerebral capillaries 90 days after fistula formation in the model group. CONCLUSION: These results demonstrated that chronic cerebral hypoperfusion could induce sustained up-regulation of VEGF mRNA and protein expression in rat brain, which was correlated with angiogenesis. An absence of corresponding astrocytic reactivity during angiogenesis may be an important factor accounting for structural deficits of the blood-brain barrier and the occurrence of normal-perfusion pressure breakthrough.

[Embolizing of high flow craniomaxillofacial arteriovenous malformations with superselected endovascular catheterization: report of 9 cases].

OBJECTIVE: Using endovascular embolization to cure and stop the enlargement of craniomaxillofacial AVMs. METHODS: Nine patients with craniomaxillofacial AVMs were treated with endovascular embolization. Among them four were males and five females. The average age was 21 years old. The diagnosis was made according to CT, MRI and DSA angiograpy. PVA particles was used via a microcatheter to embolize the AVMs. RESULTS: In this group,the lesions in six of nine patients were totally embolized by one procedure. The other three cases underwent two procedures. All the lesions were totally embolized. The follow up of eight in nine patients (except one lost) showed a good recovery of the swollen skin around the focus, the colour and the temperature became normal. No complications were observed. CONCLUSION: Endovascular embolization is an effective method to cure the lesions or to stop the enlargement of craniomaxillofacial AVMs with minimal invasion. It is important that this method can avoid damaging the face by surgical resection. We also find that the venous part or the venous pool of the fistulae is the most important part for the lesions to reoccur.