Lawton M T, Jacobowitz R, Spetzler R F
Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona, USA.
J Neurosurg. 1997 Aug;87(2):267-74. doi: 10.3171/jns.1997.87.2.0267.
To investigate the role of angiogenesis in the pathogenesis of dural arteriovenous malformations (AVMs), 40 rats underwent common carotid artery-external jugular vein (CCA-EJV) anastomosis, bipolar coagulation of the vein draining the transverse sinus, and sagittal sinus thrombosis to induce venous hypertension. Fifteen rats underwent a similar surgical procedure, but venous hypertension was not induced. The 55 rats were divided into seven groups. Four groups, each containing 10 rats, underwent induced venous hypertension. The other three groups, each containing five rats, did not undergo induced venous hypertension. After 1, 2, or 3 weeks, dura mater was obtained from one group of hypertensive rats and from one group of nonhypertensive rats and was assayed for angiogenic activity (rabbit cornea bioassay). The remaining group of 10 hypertensive rats was not assayed to determine if sampling affected dural AVM formation. Unlike rats without CCA-EJV anastomosis, rats with CCA-EJV anastomosis had significantly increased postoperative sagittal sinus pressures (p < 0.0001). Mean angiogenesis indices were significantly greater in rats with venous hypertension than in rats without venous hypertension (p = 0.004). Dural AVMs formed in 42% of the 55 rats and facial AVMs formed in 51%. Angiogenic activity correlated positively with venous hypertension (p = 0.74). Development of dural AVMs correlated positively with both venous hypertension (p = 0.0009) and angiogenic activity (p = 0.04). These data indicate that venous hypertension may induce angiogenic activity either directly or indirectly by decreasing cerebral perfusion and increasing ischemia, and that dural AVM formation may be the result of aberrant angiogenesis.
为研究血管生成在硬脑膜动静脉畸形（AVM）发病机制中的作用，对40只大鼠进行了颈总动脉-颈外静脉（CCA-EJV）吻合术、双极电凝横窦引流静脉以及矢状窦血栓形成术以诱导静脉高压。15只大鼠接受了类似的外科手术，但未诱导静脉高压。这55只大鼠被分为7组。4组，每组10只大鼠，接受诱导静脉高压。另外3组，每组5只大鼠，未接受诱导静脉高压。1、2或3周后，从一组高血压大鼠和一组非高血压大鼠获取硬脑膜，并检测其血管生成活性（兔角膜生物测定法）。剩余10只高血压大鼠组未进行检测以确定取样是否影响硬脑膜AVM形成。与未进行CCA-EJV吻合术的大鼠不同，进行CCA-EJV吻合术的大鼠术后矢状窦压力显著升高（p < 0.0001）。静脉高压大鼠的平均血管生成指数显著高于无静脉高压大鼠（p = 0.004）。55只大鼠中有42%形成了硬脑膜AVM，51%形成了面部AVM。血管生成活性与静脉高压呈正相关（p = 0.74）。硬脑膜AVM的形成与静脉高压（p = 0.0009）和血管生成活性（p = 0.04）均呈正相关。这些数据表明，静脉高压可能通过降低脑灌注和增加缺血直接或间接诱导血管生成活性，并且硬脑膜AVM的形成可能是异常血管生成的结果。
