Mechanisms of microthrombi formation after experimental subarachnoid hemorrhage

Sabri, Mohammed; Ai, Jinglu; Lakovic, Katarina; D’Abbondanza, Josephine A; Ilodigwe, Don; Macdonald, R. Loch

doi:10.1016/j.neuroscience.2012.08.002

Cited by 106 publications

(121 citation statements)

References 64 publications

Supporting

Mentioning

114

Contrasting

Order By: Relevance

“…In brief, the cWp model is technically (surgically) the most challenging model. Further, differentiation between the effects of SAH per se and effects of intracranial hypertension is not possible [18]. However, the model replicates the human pathophysiology satisfactorily, including vessel rupture and endothelial damage, which might be important features.…”

Section: Discussionmentioning

confidence: 98%

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

Muroi

Fujioka

Marbacher

et al. 2014

Acta Neurochirurgica Supplement

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 98%

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

Muroi

Fujioka

Marbacher

et al. 2014

Acta Neurochirurgica Supplement

View full text Add to dashboard Cite

show abstract

“…SAH is associated with microvascular constriction, resulting in microthrombus formation (Sabri et al, 2012) and microinfarctions (Stein et al, 2006). There is an associated global decrease in cerebral NO levels and a corresponding increase in cerebral P-selectin levels (Sabri et al, 2012).…”

Section: No Depletionmentioning

confidence: 99%

“…There is an associated global decrease in cerebral NO levels and a corresponding increase in cerebral P-selectin levels (Sabri et al, 2012). P-selectin is an endothelial cell adhesion molecule that promotes platelet aggregation and fibrin deposition (Zimmerman et al, 1992).…”

Section: No Depletionmentioning

confidence: 99%

The role of the nitric oxide pathway in brain injury and its treatment — From bench to bedside

Garry

Ezra

Rowland

et al. 2015

Experimental Neurology

319

221

View full text Add to dashboard Cite

Nitric oxide (NO) is a key signalling molecule in the regulation of cerebral blood flow. This review summarises current evidence regarding the role of NO in the regulation of cerebral blood flow at rest, under physiological conditions, and after brain injury, focusing on subarachnoid haemorrhage, traumatic brain injury, and ischaemic stroke and following cardiac arrest. We also review the role of NO in the response to hypoxic insult in the developing brain. NO depletion in ischaemic brain tissue plays a pivotal role in the development of subsequent morbidity and mortality through microcirculatory disturbance and disordered blood flow regulation. NO derived from endothelial nitric oxide synthase (eNOS) appears to have neuroprotective properties. However NO derived from inducible nitric oxide synthase (iNOS) may have neurotoxic effects. Cerebral NO donor agents, for example sodium nitrite, appear to replicate the effects of eNOS derived NO, and therefore have neuroprotective properties. This is true in both the adult and immature brain. We conclude that these agents should be further investigated as targeted pharmacotherapy to protect against secondary brain injury.

show abstract

“…Immunofluorescence staining was performed as previously described. 12 Sections were deparaffinized and rehydrated, followed by antigen retrieval in a 961C water bath for 25 minutes using Vector antigen unmasking solution (Vector Laboratories, Burlingame, CA, USA). Sections were permeabilized with 0.3% Triton X-100 for 15 minutes and blocked by incubating with 10% normal goat serum in 1% BSA for 60 minutes.…”

Section: Double Immunofluorescence Stainingmentioning

confidence: 99%

“…There are reports that microthrombi mediating focal ischemia are likely formed in situ rather than from the breakdown of distal larger emboli, and that these microthrombi were accompanied by arteriolar vasoconstriction. 12 If the hippocampal changes are not due to ischemia, then they must be mediated by the subarachnoid blood. In the current model, the blood was injected in the prechiasmatic cistern.…”

Section: New Findingsmentioning

confidence: 99%

Molecular Alterations in the Hippocampus after Experimental Subarachnoid Hemorrhage

Han

Wan

Kudo

et al. 2013

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Patients with aneurysmal subarachnoid hemorrhage (SAH) frequently have deficits in learning and memory that may or may not be associated with detectable brain lesions. We examined mediators of long-term potentiation after SAH in rats to determine what processes might be involved. There was a reduction in synapses in the dendritic layer of the CA1 region on transmission electron microscopy as well as reduced colocalization of microtubule-associated protein 2 (MAP2) and synaptophysin. Immunohistochemistry showed reduced staining for GluR1 and calmodulin kinase 2 and increased staining for GluR2. Myelin basic protein staining was decreased as well. There was no detectable neuronal injury by Fluoro-Jade B, TUNEL, or activated caspase-3 staining. Vasospasm of the large arteries of the circle of Willis was mild to moderate in severity. Nitric oxide was increased and superoxide anion radical was decreased in hippocampal tissue. Cerebral blood flow, measured by magnetic resonance imaging, and cerebral glucose metabolism, measured by positron emission tomography, were no different in SAH compared with control groups. The results suggest that the etiology of loss of LTP after SAH is not cerebral ischemia but may be mediated by effects of subarachnoid blood such as oxidative stress and inflammation.

show abstract

Mechanisms of microthrombi formation after experimental subarachnoid hemorrhage

Cited by 106 publications

References 64 publications

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

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

The role of the nitric oxide pathway in brain injury and its treatment — From bench to bedside

Molecular Alterations in the Hippocampus after Experimental Subarachnoid Hemorrhage

Contact Info

Product

Resources

About