Abstract T P236: Hemodynamic Changes May Be Partly Attributable To The Formation And Rupture Of Aneurysms In A Rat Model
Introduction: To prevent subarachnoid hemorrhage (SAH), its pathogenesis must be understood. SAH and cerebral aneurysms are located at vascular walls exposed to hemodynamic stress and turbulence. In our experimental aneurysm model, rats were subjected to oophorectomy, right common carotid artery ligation (CCA), and bilateral posterior renal ligation; they received a high-salt diet. Although we noted a high incidence of aneurysms at the anterior cerebral artery-olfactory artery (ACA-OA) bifurcation, no SAH occurred at this site. As hemodynamic changes are thought to stimulate the vascular wall locally, we hypothesized that additive hemodynamic changes lead to the development and rupture of cerebral aneurysms.
Methods: We divided 42 rats into 3 groups, group A (n=26) underwent ligation of the right CCA, in group B (n=10) we ligated the right pterygopalatine artery, the right external carotid artery, and the left CCA, and in group C (n=6) we additionally ligated the bilateral vertebral arteries.
Results: In the 12 weeks after aneurysm induction, 5 group A (19%)-, 3 group B (30%)-, and 3 group C (50%) rats suffered aneurysmal rupture. As in humans, the ruptured aneurysms were primarily located at the anterior communicating artery, the posterior communicating artery, and the internal carotid-posterior communicating artery. There were no ruptured aneurysms at the ACA-OA bifurcation.
Conclusion: Our findings suggest that hemodynamic changes are at least partly associated with the vulnerability of the vascular wall at the circle of Willis. Studies are underway to identify the mechanisms underlying the pathologic vascular changes.
Author Disclosures: T. Miyamoto: None. M. Kohrai: None. D.K. Kung: None. K.T. Kitazato: None. K. Shimada: None. K. Yagi: None. Y. Tada: None. Y. Kurashiki: None. K. Kuwayama: None. J. Satomi: None. S. Nagahiro: None.
- © 2015 by American Heart Association, Inc.