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

硬脑膜动静脉瘘(DAVF)发生发展的确切机制尚不清楚，但已推测血管新生生长因子可能参与其发病机制。此外，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。本研究旨在探讨脑室注射脑源性神经营养因子(BDNF)对大鼠脑静脉闭塞(2-VO)模型脑静脉缺血灶的梗塞范围、细胞凋亡的抑制作用及对局部脑血流的影响。结果显示，脑源性神经营养因子治疗组与对照组的rCBF差异无统计学意义。结果发现，2-VO后，BDNF治疗组2天和7天的平均脑梗塞体积分别为1.49±1.44%和0.93±0.47%，明显小于对照组的3.66±1.51%和1.69±0.58%(P<0.05)。2-VO后2天，BDNF治疗组大鼠肝组织TUNEL阳性细胞数(17.0±15.1)较对照组(39.0±19.6)明显减少(P<0.05)。上述结果提示，脑室持续给予BDNF可保护大鼠大脑皮质细胞凋亡，缩小脑梗塞面积，但对局部脑血流无明显影响。

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.