A model of the pathophysiology of cerebral arteriovenous malformations by a carotid-jugular fistula in the rat.

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.