Platelet and Leukocyte Adhesion in the Microvasculature at the Cerebral Surface Immediately After Subarachnoid Hemorrhage

Ishikawa, Mami; Kusaka, Gen; Yamaguchi, Noriyuki; Sekizuka, Eiichi; Nakadate, Hiromichi; Minamitani, Haruyuki; Shinoda, Souji; Watanabe, Eiju

doi:10.1227/01.neu.0000337579.05110.f4

Cited by 79 publications

(65 citation statements)

References 22 publications

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“…The few published in vivo studies investigating the cerebral microcirculation after SAH used conventional epifluorescence microscopy and were due to the limited penetration depth of this technology limited to pial vessels. [36][37][38] These vessels were of specific interest in the context of SAH since these are the only cerebral microvessels coming in direct contact with extravasated blood after subarachnoid bleeding. Indeed, pial vessels were shown to constrict after SAH in experimental animals models and in SAH patients thereby suggesting that spasms of cerebral microvessels are one of the main reasons for the cerebral ischemia observed after SAH.…”

Section: Discussionmentioning

confidence: 99%

Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo

Balbi¹,

Koide

Schwarzmaier³

et al. 2016

J Cereb Blood Flow Metab

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Subarachnoid hemorrhage causes acute and long-lasting constrictions of pial arterioles. Whether these vessels dilate normally to neuronal activity is of great interest since a mismatch between delivery and consumption of glucose and oxygen may cause additional neuronal damage. Therefore, we investigated neurovascular reactivity of pial and parenchymal arterioles after experimental subarachnoid hemorrhage. C57BL/6 mice were subjected to subarachnoid hemorrhage by filament perforation or sham surgery. Neurovascular reactivity was assessed 3 h later by forepaw stimulation or inhalation of 10% CO 2 . Diameters of cerebral arterioles were assessed using two-photon microscopy. Neurovascular coupling and astrocytic endfoot Ca 2þ were measured in brain slices using two-photon and infrared-differential interference contrast microscopy. Vessels of sham-operated mice dilated normally to CO 2 and forepaw stimulation. Three hours after subarachnoid hemorrhage, CO 2 reactivity was completely lost in both pial and parenchymal arterioles, while neurovascular coupling was not affected. Brain slices studies also showed normal neurovascular coupling and a normal increase in astrocytic endfoot Ca 2þ acutely after subarachnoid hemorrhage. These findings suggest that communication between neurons, astrocytes, and parenchymal arterioles is not affected in the first few hours after subarachnoid hemorrhage, while CO 2 reactivity, which is dependent on NO signaling, is completely lost.

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Section: Discussionmentioning

confidence: 99%

Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo

Balbi¹,

Koide

Schwarzmaier³

et al. 2016

J Cereb Blood Flow Metab

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show abstract

“…Finally, the current study was performed in a recently improved mouse SAH model (Feiler et al, 2010). Mice have a translucent dura mater and therefore allow the visualization of the subarachnoid/pial microcirculation without durotomy (Kataoka et al, 2004;Ishikawa et al, 2009;Schwarzmaier et al, 2010). This means that the cerebral microcirculation can be visualized without any previous mechanical alterations to the cerebral vasculature and under conditions of physiological cerebrospinal fluid flow.…”

Section: Discussionmentioning

confidence: 99%

Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

Friedrich

Müller

Feiler

et al. 2011

J Cereb Blood Flow Metab

191

196

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Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is characterized by a severe, cerebral perfusion pressure (CPP)-independent reduction in cerebral blood flow suggesting alterations on the level of cerebral microvessels. Therefore, we aimed to use in-vivo imaging to investigate the cerebral microcirculation after experimental SAH. Subarachnoid hemorrhage was induced in C57/BL6 mice by endovascular perforation. Pial arterioles and venules (10 to 80 lm diameter) were examined using in-vivo fluorescence microscopy, 3, 6, and 72 hours after SAH. Venular diameter or flow was not affected by SAH, while > 70% of arterioles constricted by 22% to 33% up to 3 days after hemorrhage (P < 0.05 versus sham). The smaller the investigated arterioles, the more pronounced the constriction (r 2 = 0.92, P < 0.04). Approximately 30% of constricted arterioles were occluded by microthrombi and the frequency of arteriolar microthrombosis correlated with the degree of constriction (r 2 = 0.93, P < 0.03). The current study demonstrates that SAH induces microarterial constrictions and microthrombosis in vivo. These findings may explain the early CPP-independent decrease in cerebral blood flow after SAH and may therefore serve as novel targets for the treatment of early perfusion deficits after SAH.

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“…No model other than the cWp model reflects the latter aspect. Furthermore, the superiority of the cWp model to reproduce early platelet-leukocyteendothelial cell interactions after SAH has been described more recently [7].…”

Section: Discussionmentioning

confidence: 99%

Mouse Model of Subarachnoid Hemorrhage: Technical Note on the Filament Perforation Model

Muroi

Fujioka

Marbacher

et al. 2014

Acta Neurochirurgica Supplement

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Experiments using genetically engineered mice are regarded as indispensable to gaining a better understanding of the molecular pathophysiology in neuronal injury after subarachnoid hemorrhage (SAH). Therefore, mouse SAH models are becoming increasingly important. The circle of Willis perforation (cWp) model is the most frequently used mouse SAH model. We report and discuss the technical surgical approach, results, and difficulties associated with the cWp model, with reference to the existing literature. Our results largely confirmed previously published results. This model may be the first choice at present, because important pathologies can be reproduced in this model and most findings in the literature are based on it. AbstractExperiments using genetically engineered mice are regarded as indispensable to gaining a better understanding of the molecular pathophysiology in neuronal injury after subarachnoid hemorrhage (SAH). Therefore, mouse SAH models are becoming increasingly important. The circle of Willis perforation (cWp) model is the most frequently used mouse SAH model. We report and discuss the technical surgical approach, results, and difficulties associated with the cWp model, with reference to the existing literature. Our results largely confirmed previously published results. This model may be the first choice at present, because important pathologies can be reproduced in this model and most findings in the literature are based on it.

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Platelet and Leukocyte Adhesion in the Microvasculature at the Cerebral Surface Immediately After Subarachnoid Hemorrhage

Abstract: SAH at the skull base induced P-selectin- and oxygen radical-mediated platelet-leukocyte-endothelial cell interactions in venules at the cerebral surface. These early inflammatory and prothrombogenic responses may cause a whole-brain injury immediately after SAH.

Cited by 79 publications

References 22 publications

Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo

Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo

Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study

Mouse Model of Subarachnoid Hemorrhage: Technical Note on the Filament Perforation Model

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