Filament perforation model for mouse subarachnoid hemorrhage: Surgical-technical considerations

Muroi, Carl; Fujioka, Masayuki; Okuchi, Kazuo; Fandiño, Javier; Keller, Emanuela; Sakamoto, Yuya; Mishima, Kenichi; Iwasaki, Katsunori; Fujiwara, Michihiro

doi:10.3109/02688697.2014.918579

Cited by 27 publications

(26 citation statements)

References 49 publications

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“…In addition, perfusion was examined in vivo, whereas vasospasm was analyzed ex vivo. The time point of 72 h was chosen because our data and other studies have reported that vasospasm peaks 72 h after induction of SAH in the murine endovascular filament perforation model [16,23,24]. Although we cannot rule out that a correlation between vasospasm and cortical perfusion may have been present at earlier time points, the lack of correlation at 72 h indicates that large vessel vasospasm is of limited relevance in the murine model.…”

Section: Discussionmentioning

confidence: 98%

“…This time point was selected to determine the impact on cortical perfusion at the peak of CV [16,23,24]. We analyzed the vessel volume of a 2.5-mm vessel segment of the left MCA distal of the carotid T, which is a highly sensitive parameter for evaluating vasospasm [28].…”

Section: Sah Induces Vasospasmmentioning

confidence: 99%

“…Although these changes occur with faster temporal dynamics in mice than humans-peaking 3 days after SAH in mice [16,23,24] compared to 7 to 10 days in humans [3]-murine models have become an important tool for basic research on the pathophysiology of SAH. The majority of experimental studies to date have focused on CV [12][13][14][15][16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

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Large Vessel Vasospasm Is Not Associated with Cerebral Cortical Hypoperfusion in a Murine Model of Subarachnoid Hemorrhage

Neulen

Meyer

Kramer

et al. 2018

Transl. Stroke Res.

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Clinical studies on subarachnoid hemorrhage (SAH) have shown discrepancies between large vessel vasospasm, cerebral perfusion, and clinical outcome. We set out to analyze the contribution of large vessel vasospasm to impaired cerebral perfusion and neurological impairment in a murine model of SAH. SAH was induced in C57BL/6 mice by endovascular filament perforation. Vasospasm was analyzed with microcomputed tomography, cortical perfusion by laser SPECKLE contrast imaging, and functional impairment with a quantitative neuroscore. SAH animals developed large vessel vasospasm, as shown by significantly lower vessel volumes of a 2.5-mm segment of the left middle cerebral artery (MCA) (SAH 5.6 ± 0.6 nL, sham 8.3 ± 0.5 nL, p < 0.01). Induction of SAH significantly reduced cerebral perfusion of the corresponding left MCA territory compared to values before SAH, which only recovered partly (SAH vs. sham, 15 min 35.7 ± 3.1 vs. 101.4 ± 10.2%, p < 0.01; 3 h, 85.0 ± 8.6 vs. 121.9 ± 13.4, p < 0.05; 24 h, 75.3 ± 4.6 vs. 110.6 ± 11.4%, p < 0.01; 72 h, 81.8 ± 4.8 vs. 108.5 ± 14.5%, n.s.). MCA vessel volume did not correlate significantly with MCA perfusion after 72 h (r = 0.34, p = 0.25). Perfusion correlated moderately with neuroscore (24 h: r = − 0.58, p < 0.05; 72 h: r = − 0.44, p = 0.14). There was no significant correlation between vessel volume and neuroscore after 72 h (r = − 0.21, p = 0.50). In the murine SAH model, cerebral hypoperfusion occurs independently of large vessel vasospasm. Neurological outcome is associated with cortical hypoperfusion rather than large vessel vasospasm.

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Section: Discussionmentioning

confidence: 98%

Section: Sah Induces Vasospasmmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Large Vessel Vasospasm Is Not Associated with Cerebral Cortical Hypoperfusion in a Murine Model of Subarachnoid Hemorrhage

Neulen

Meyer

Kramer

et al. 2018

Transl. Stroke Res.

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“…1 The endovascular perforation method for inducing SAH is frequently used in rodents, and is considered to the closest imitation of human SAH. 2,3 In that model, there are greater inter-animals variations in the extent and volume of subarachnoid clot compared to other SAH models.…”

mentioning

confidence: 99%

New Grading System Based on Magnetic Resonance Imaging in a Mouse Model of Subarachnoid Hemorrhage

Egashira

Shishido

Hua

et al. 2015

Stroke

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Background and Purpose A grading system for experimental subarachnoid hemorrhage (SAH) that does not require animal euthanasia is currently unavailable. We proposed a new grading system based on magnetic resonance imaging (MRI), and evaluated the feasibility of this method in a mouse model of SAH. Methods SAH was induced by endovascular perforation in adult male C57BL/6 mice. Mice underwent MRI 24 hours after SAH, and were categorized into the following five grades based on T2*-weighted imaging: Grade 0, no visible SAH or intraventricular hemorrhage (IVH); Grade 1, minimal/localized SAH without IVH; Grade 2, minimal/localized SAH with IVH; Grade 3, thick/diffuse SAH without IVH; Grade 4, thick/diffuse SAH with IVH. Neurological deficits were then assessed and the mice euthanized for conventional SAH grading. Results Among a total of 47 mice, 4% were scored as grade 0, 30% as grade 1, 11% as grade 2, 30% as grade 3, and 36% as grade 4. This MRI grading had excellent interobserver reliability (weighted κ value = 0.94), and there were strong correlations between the MRI grading and the conventional grading (r = 0.85; P < 0.001), or between MRI grade and neurological scores (r = −0.46; P < 0.01). Conclusions The new MRI grading correlated well with conventional grading, and enabled in-vivo evaluation of SAH severity. This grading system may offer advantages in future studies of experimental SAH.

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“…Male Sprague-Dawley rats (SD rats) weighing 300 to 350 g (8–10 weeks old) were used in this study, and the endovascular perforation model of SAH was implemented in rats as described previously47. Briefly, SD rats were anesthetized with 5% isoflurane, and then were positioned in a supine position.…”

Section: Methodsmentioning

confidence: 99%

PPARβ/δ, a Novel Regulator for Vascular Smooth Muscle Cells Phenotypic Modulation and Vascular Remodeling after Subarachnoid Hemorrhage in Rats

Zhang

Jiang

Guo

et al. 2017

Sci Rep

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Cerebral vascular smooth muscle cell (VSMC) phenotypic switch is involved in the pathophysiology of vascular injury after aneurysmal subarachnoid hemorrhage (aSAH), whereas the molecular mechanism underlying it remains largely speculative. Peroxisome proliferator-activated receptor β/δ (PPARβ/δ) has been implicated to modulate the vascular cells proliferation and vascular homeostasis. In the present study, we investigated the potential role of PPARβ/δ in VSMC phenotypic switch following SAH. Activation of PPARβ/δ by GW0742 and adenoviruses PPARβ/δ (Ad-PPARβ/δ) significantly inhibited hemoglobin-induced VSMC phenotypic switch. However, the effects of PPARβ/δ on VSMC phenotypic switch were partly obstacled in the presence of LY294002, a potent inhibitor of Phosphatidyl-Inositol-3 Kinase-AKT (PI3K/AKT). Furthermore, following study demonstrated that PPARβ/δ-induced PI3K/AKT activation can also contribute to Serum Response Factor (SRF) nucleus localization and Myocardin expression, which was highly associated with VSMC phenotypic switch. Finally, we found that Ad-PPARβ/δ positively modulated vascular remodeling in SAH rats, i.e. the diameter of basilar artery and the thickness of vessel wall. In addition, overexpression of PPARβ/δ by adenoviruses significantly improved neurological outcome. Taken together, this study identified PPARβ/δ as a useful regulator for VSMC phenotypic switch and vascular remodeling following SAH, providing novel insights into the therapeutic strategies of delayed cerebral ischemia.

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Filament perforation model for mouse subarachnoid hemorrhage: Surgical-technical considerations

Abstract: The current study provides additional useful information characterizing the cWp model. This model may be of first choice at present, as important pathologies can be reproduced and most findings in the literature are based on it.

Cited by 27 publications

References 49 publications

Large Vessel Vasospasm Is Not Associated with Cerebral Cortical Hypoperfusion in a Murine Model of Subarachnoid Hemorrhage

Large Vessel Vasospasm Is Not Associated with Cerebral Cortical Hypoperfusion in a Murine Model of Subarachnoid Hemorrhage

New Grading System Based on Magnetic Resonance Imaging in a Mouse Model of Subarachnoid Hemorrhage

PPARβ/δ, a Novel Regulator for Vascular Smooth Muscle Cells Phenotypic Modulation and Vascular Remodeling after Subarachnoid Hemorrhage in Rats

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