Given the poor outcome of subarachnoid hemorrhage due to rupture of intracranial aneurysms (IAs) and high prevalence of IAs in general public, elucidation of mechanisms underlying the pathogenesis of the disease and development of effective treatment are mandatory for social health. Recent experimental findings have revealed the crucial contribution of macrophage-mediated chronic inflammation to and greatly promoted our understanding of the pathogenesis. Also a series of studies have proposed the potential of anti-inflammatory drugs as therapeutic ones. In this process, a rodent model of IAs plays an indispensable role. Basic concept of IA induction in such kind of models is that IA formation is triggered by hemodynamic stress loaded on damaged arterial walls. To be more precise, although detailed procedures are different among researchers, animals are subjected to a ligation of a unilateral carotid artery and systemic hypertension achieved by a salt overloading, and IAs are induced at the contralateral bifurcation site. Importantly, trigger of IA formation in the model mimics human one, and IA lesions induced share similarity in histology with human ones such as degenerative changes of media. For further elucidating the pathogenesis, we need to well understand variations, usefulness, and also limits of this model.
Keywords: Animal model; Chronic inflammation; Hemodynamic stress; Intracranial aneurysm; Macrophage; Subarachnoid hemorrhage.