Morgan M K, Anderson R E, Sundt T M
Department of Neurologic Surgery, Mayo Clinic, Rochester, MN.
Brain Res. 1989 Sep 4;496(1-2):241-50. doi: 10.1016/0006-8993(89)91071-8.
A model of a carotid-jugular fistula in the rat was created such that the arterial feeding vessel is derived from the intracranial arterial circulation and the venous drainage communicates with a major intracranial venous drainage system. This fistula was created in 28 rats on the right side with an additional 11 rats designed as controls with a right carotid ligation and 6 rats without previous surgery. After 12 weeks convalescence, 6 rats with a carotid-jugular fistula and 6 rats without previous surgery underwent cerebral angiography. All fistulae were patent and the model was verified. All of the 33 remaining rats underwent regional cerebral blood flow (rCBF) determination by [14C]iodoantipyrine autoradiography under barbiturate anesthesia. Of the rats with the fistula, 11 had this fistula obliterated 5 min prior to rCBF determination ('closed' group) while 11 had rCBFs determined with the fistula ('open' group). The rCBF was measured from each hemisphere from 7 anatomical regions. The rCBF in the control animals ranged from a median of 82 to 112 ml/100 g/min, in the 'open fistula' group 46 to 68 ml/100 g/min, and in the 'closed' group 118 to 187 ml/100 g/min. This experimental model stimulates the pathophysiologic perturbations in the parenchyma induced by cerebral arteriovenous malformations. It supports the findings that non-infarctional hypoperfusion can result from arteriovenous malformations and that following extirpation of arteriovenous malformations hyperemia may ensue.
构建了大鼠颈静脉瘘模型，使动脉供血血管源自颅内动脉循环，静脉引流与主要的颅内静脉引流系统相通。在28只大鼠右侧制造了这种瘘管，另有11只大鼠作为对照组，进行右侧颈动脉结扎，还有6只大鼠未接受过手术。恢复12周后，对6只患有颈静脉瘘的大鼠和6只未接受过手术的大鼠进行了脑血管造影。所有瘘管均通畅，模型得到验证。其余33只大鼠均在巴比妥类麻醉下通过[14C]碘安替比林放射自显影法测定局部脑血流量（rCBF）。在患有瘘管的大鼠中，11只在测定rCBF前5分钟闭塞了瘘管（“闭合”组），而11只在瘘管存在的情况下测定了rCBF（“开放”组）。从7个解剖区域测量每个半球的rCBF。对照动物的rCBF中位数范围为82至112 ml/100 g/min，“开放瘘管”组为46至68 ml/100 g/min，“闭合”组为118至187 ml/100 g/min。该实验模型模拟了脑动静脉畸形引起的实质内病理生理紊乱。它支持以下发现：动静脉畸形可导致非梗死性灌注不足，动静脉畸形切除后可能会出现充血。
