Terada T, Higashida R T, Halbach V V, Dowd C F, Tsuura M, Komai N, Wilson C B, Hieshima G B
Department of Radiology, University of California Medical Center, San Francisco.
J Neurosurg. 1994 May;80(5):884-9. doi: 10.3171/jns.1994.80.5.0884.
Dural sinus thrombosis has been hypothesized as a possible cause of dural arteriovenous fistulas (AVF's). The pathogenesis and evolution from thrombosis to actual development of an AVF are still unknown. To study dural fistula formation, a surgically induced venous hypertension model in rats was created by producing an arteriovenous shunt between the carotid artery and the external jugular vein. The external jugular vein beyond the anastomosis was ligated 2 to 3 months after surgery and angiography was performed to identify any new acquired AVF's. Forty-six male Sprague-Dawley rats, each weighing approximately 300 gm, were used for this study. In Group I, 22 rats underwent a common carotid artery anastomosis to the external jugular vein, which is the largest draining vein from the transverse sinus via the posterior facial vein, followed by proximal external jugular vein ligation. In Group II, 13 rats underwent the same surgical procedure, followed by contralateral posterior facial vein occlusion. Group III served as the control group, in which 11 rats underwent only unilateral external jugular vein occlusion with or without contralateral posterior facial vein occlusion. The shunts in Groups I and II were ligated at 2 to 3 months following surgery, and transfemoral angiography was performed immediately before and after occlusion. New acquired AVF's had developed in three rats (13.6%) in Group I, three rats (23.1%) in Group II, and no rats (0%) in Group III. One of these newly formed fistulas was located at the dural sinus, analogous to the human dural AVF. The other five were located in the subcutaneous tissue, including the face and neck. The dural AVF in the rat was present on follow-up angiography at 1 week after the bypass occlusion. It is concluded that chronic venous hypertension of 2 to 3 months' duration, without associated venous or sinus thrombosis, can induce new AVF's affecting the dural sinuses or the subcutaneous tissue.
硬脑膜窦血栓形成被认为是硬脑膜动静脉瘘(AVF)的一个可能病因。从血栓形成到AVF实际发生的发病机制和演变过程仍不清楚。为了研究硬脑膜瘘的形成,通过在大鼠颈动脉和颈外静脉之间建立动静脉分流,创建了一种手术诱导的静脉高压模型。术后2至3个月结扎吻合口远端的颈外静脉,并进行血管造影以确定是否有新形成的获得性AVF。本研究使用了46只体重约300克的雄性Sprague-Dawley大鼠。在第一组中,22只大鼠接受了颈总动脉与颈外静脉的吻合,颈外静脉是从横窦经面后静脉引流的最大静脉,随后结扎近端颈外静脉。在第二组中,13只大鼠接受了相同的手术操作,随后结扎对侧的面后静脉。第三组作为对照组,11只大鼠仅接受单侧颈外静脉结扎,伴或不伴有对侧的面后静脉结扎。第一组和第二组的分流在术后2至3个月结扎,在闭塞前后立即进行经股动脉血管造影。第一组有3只大鼠(13.6%)、第二组有3只大鼠(23.1%)出现了新形成的获得性AVF,第三组没有大鼠(0%)出现。这些新形成的瘘管中有1个位于硬脑膜窦,类似于人类的硬脑膜AVF。另外5个位于皮下组织,包括面部和颈部。在旁路闭塞后1周的随访血管造影中发现大鼠存在硬脑膜AVF。结论是,持续2至3个月的慢性静脉高压,无相关的静脉或窦血栓形成,可诱发影响硬脑膜窦或皮下组织的新AVF。