Study on the treatment of dural arteriovenous fistula by the inhibition of angiogenic growth factors

硬脑膜动静脉瘘（DAVF）发生和生长的确切机制尚不清楚，但据推测，血管血管生成生长因子可能参与发病机制。脑源性神经营养因子（BDNF）对局部脑血流量（rCBF）的影响以及对脑静脉缺血的神经保护作用尚不清楚。本研究旨在观察脑室内注射BDNF对大鼠2-VO模型脑静脉缺血损伤的梗死范围、细胞凋亡的抑制作用及对局部脑血流量的影响。结果显示，BDNF处理组和对照组之间的rCBF无统计学差异。结果发现，在2-VO后，BDNF治疗的动物的平均梗死体积在2天（1.49±1.44%）和7天（0.93±0.47%）显著小于对照组（v.s.3.66± 1.51%，P<0.05）。1.69± 0.58%，P<0.05）。2-VO后2d，BDNF组TUNEL阳性细胞数（17.0±15.1）明显少于对照组（39.0±19.6），P<0.05。结果提示，脑室内持续给予BDNF可保护大鼠静脉性脑梗死模型脑皮质的凋亡改变，缩小梗死面积，而对rCBF无影响。

The precise mechanisms responsible for the development and growth of dural arteriovenous fistula (DAVF) remain unclear, but it has been hypothesized that vascular angiogenic growth factors might be involved in the pathogenesis. Also, it remains unknown that Brain-Derived Neurotrophic Factor (BDNF) effect on regional Cerebral Blood Flow (rCBF) and has neuroprotective effect in cerebral venous ischemia. The present study was undertaken to investigate whether intraventricular BDNF infusion effects on infarct size and suppression of apoptosis in cerebral venous ischemic lesion in a rat 2-vein occlusion (2-VO) model and effect on rCBF. As the results, there were no statistical differences in rCBF between BDNF-treated and control groups. It was found that the mean infarct volumes after 2-VO were significantly smaller in BDNF-treated animals than controls at 2 days (1.49±1.44% v.s.3.66±1.51%, P<0.05) and 7 days (0.93±0.47% v.s. 1.69±0.58%, P<0.05). The number of TUNEL positive cells detected at 2 days after 2-VO was significantly fewer in BDNF-treated animals (17.0±15.1) than controls (39.0±19.6, P<0.05). These results suggest that continuous intraventricular administration of BDNF protects apoptotic change of brain cortex and reduced infarct size without effect on rCBF in rat venous infarction model.