Introduction: To study the pathomechanisms of cerebral aneurysms, we developed a rat model of cerebral aneurysm rupture. In order, the ruptured aneurysms were located at the P1 segment of the left posterior cerebral artery, on the anterior cerebral artery (ACA), the right internal carotid artery (ICA), the right middle cerebral artery (MCA), and the anterior communicating artery (AcomA). We investigated the early morphological changes in these arteries that preceded aneurysm formation.
Methods: We subjected 10-week-old Sprague-Dawley rats to bilateral ovariectomy and modified carotid artery ligation. They were fed a high salt diet. Two weeks later, the bilateral posterior renal arteries were ligated. Vascular corrosion casts were created 2 weeks after renal artery ligation (n=11) and the morphological features were compared on casts from these- and sham rats (n=3) using a scanning electron microscope.
Results: The diameter of the left- was larger than of the right P1 in all rats with hypertension and estrogen deficiency. Endothelial changes were predominantly seen in the AcomA and the left P1. In 5 rats we observed small protrusions without loss of endothelial imprints suggesting local loss of internal elastic lamina in the left P1 where ruptured aneurysms were frequently formed. No aneurysms formed at the right ACA-olfactory artery (OA) bifurcation within 2 weeks after aneurysm induction. None of these changes were found in the controls. As ACA-OA aneurysms were frequently seen at 3 months but never ruptured, the pathophysiology of such, and of aneurysms formed at other sites may be different.
Conclusion: We first demonstrate the initial morphological changes that occurred as early as two weeks after aneurysm induction in rats. Early intervention for hypertension and endothelial damage may be beneficial in the management of cerebral aneurysms.