Fig. 12.1
Representative intracranial aneurysms in mice. Left panel: Normal cerebral artery. Middle panel: Unruptured aneurysm in the right anterior cerebral artery. Right panel: Ruptured aneurysm with subarachnoid hemorrhage in the right middle cerebral artery. Cerebral arteries were visualized by blue dyes dissolved in gelatin. Arrows indicate aneurysms. Bar = 2.5 mm (Reprinted by permission from Macmillan Publishers Ltd: Journal of Cerebral Blood Flow and Metabolism (Shimada et al. [7]), copyright 2015)
However, to induce intracranial aneurysms and aneurysmal rupture consistently, accurate stereotaxic procedure to inject elastase into the cerebrospinal fluid at the right basal cistern is critical [12]. This is one of the limitations of our model. Because exogenous elastase was used to induce aneurysms in our model, the early step of aneurysm formation that requires endogenous elastase may have been bypass.
In this model, the mechanisms of aneurysmal formation and rupture and the possible pharmacological therapy for the prevention of aneurysmal rupture can be studies for future studies that utilized various inhibitors, knockout mice, or transgenic mice.
Sources of Funding
This study was funded by National Institutes of Health (NIH) R01NS055876 (to T.H.), R01NS082280 (to T.H.).
There are no conflicts of interest.
Disclosures
None.
References
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Nuki Y, Tsou TL, Kurihara C, Kanematsu M, Kanematsu Y, Hashimoto T. Elastase-induced intracranial aneurysms in hypertensive mice. Hypertension. 2009;54:1337–44.PubMedCentralCrossRefPubMed
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Kanematsu Y, Kanematsu M, Kurihara C, Tada Y, Tsou TL, van Rooijen N, et al. Critical roles of macrophages in the formation of intracranial aneurysm. Stroke. 2011;42:173–8.PubMedCentralCrossRefPubMed
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