A Modification to a Murine Model for Intracranial Aneurysm Formation and Rupture.
A Modification to a Murine Model for Intracranial Aneurysm Formation and Rupture.
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DOI：
10.7759/cureus.16250
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发表时间：
2021-07
期刊：
影响因子：
--
通讯作者：
Hoh BL
中科院分区：
文献类型：
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作者：
Patel D;Dodd WS;Motwani K;Hosaka K;Hoh BL
3.6%至6.0%的人群患有颅内动脉瘤。颅内动脉瘤形成和破裂的机制尚不完全清楚。已经开发了几种啮齿动物模型，以更好地了解颅内动脉瘤的病理生理学。高血压、血流动力学变化和血管损伤都是动脉瘤诱导所必需的;然而，多种侵入性手术可能会破坏动物的生理机能。因此，我们假设我们诱导高血压的方法可以修改以创建更简单的模型。我们以前开发了一种高度可重复的颅内动脉瘤形成和破裂的小鼠模型，该模型涉及通过结扎左颈总动脉、使用弹性蛋白酶和赖氨酰氧化酶抑制剂的血管壁降解以及通过高盐饮食、连续血管紧张素II输注和右肾动脉结扎的高血压的血流动力学变化。为了建立一个更简单的模型，我们试图消除肾动脉结扎。我们评估了C57 BL/6小鼠的两个单独队列中的动脉瘤形成、动脉瘤破裂和血压：一个队列接受如上所述的我们的模型，而另一个队列不接受右肾动脉结扎。我们的研究结果表明，颅内动脉瘤形成和破裂率在各组之间没有差异。此外，在模型的不同时间点，队列之间的血压没有差异。然而，两个队列的血压均较基线显著升高，表明诱导高血压不需要肾动脉结扎。这些发现表明，我们的小鼠模型可以修改，以消除右肾动脉结扎。因此，我们建议对我们的小鼠模型进行修改，以研究颅内动脉瘤病理生理学。
Between 3.6% and 6.0% of the population has an intracranial aneurysm. The mechanisms underlying intracranial aneurysm formation and rupture are not fully known. Several rodent models have been developed to better understand intracranial aneurysm pathophysiology. Hypertension, hemodynamic changes, and vessel injury are all necessary for aneurysm induction; however, multiple invasive procedures may disrupt an animal’s physiology. Therefore, we hypothesized that our method for inducing hypertension could be modified to create a simpler model. We previously developed a highly reproducible murine model of intracranial aneurysm formation and rupture that involves hemodynamic changes through ligation of the left common carotid artery, vessel wall degradation using elastase and a lysyl oxidase inhibitor, and hypertension through a high-salt diet, continuous angiotensin II infusion, and right renal artery ligation. In order to create a simpler model, we sought to eliminate renal artery ligation. We assessed aneurysm formation, aneurysm rupture, and blood pressure in two separate cohorts of C57BL/6 mice: one cohort underwent our model as above, while another cohort did not receive right renal artery ligation. Our results demonstrate that intracranial aneurysm formation and rupture rates did not differ between each group. Further, the blood pressures between cohorts did not differ at various timepoints in the model. Both cohorts, however, did have a significant increase in blood pressure from baseline, suggesting that renal artery ligation is not needed for inducing hypertension. These findings demonstrate that our murine model can be modified to eliminate right renal artery ligation. Thus, we propose this modification to our murine model for studying intracranial aneurysm pathophysiology.