The Role of Microclot Formation in an Acute Subarachnoid Hemorrhage Model in the Rabbit

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The Role of Microclot Formation in an Acute Subarachnoid Hemorrhage Model in the Rabbit

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Title: The Role of Microclot Formation in an Acute Subarachnoid Hemorrhage Model in the Rabbit
Author: Andereggen, Lukas; Neuschmelting, Volker; von Gunten, Michael; Widmer, Hans Rudolf; Fandino, Javier; Marbacher, Serge

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Citation: Andereggen, Lukas, Volker Neuschmelting, Michael von Gunten, Hans Rudolf Widmer, Javier Fandino, and Serge Marbacher. 2014. “The Role of Microclot Formation in an Acute Subarachnoid Hemorrhage Model in the Rabbit.” BioMed Research International 2014 (1): 161702. doi:10.1155/2014/161702. http://dx.doi.org/10.1155/2014/161702.
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Abstract: Background. Microvascular dysfunction and microthrombi formation are believed to contribute to development of early brain injury (EBI) after aneurysmal subarachnoid hemorrhage (SAH). Objective. This study aimed to determine (i) extent of microthrombus formation and neuronal apoptosis in the brain parenchyma using a blood shunt SAH model in rabbits; (ii) correlation of structural changes in microvessels with EBI characteristics. Methods. Acute SAH was induced using a rabbit shunt cisterna magna model. Extent of microthrombosis was detected 24 h post-SAH (n = 8) by fibrinogen immunostaining, compared to controls (n = 4). We assessed apoptosis by terminal deoxynucleotidyl transferase nick end labeling (TUNEL) in cortex and hippocampus. Results. Our results showed significantly more TUNEL-positive cells (SAH: 115 ± 13; controls: 58 ± 10; P = 0.016) and fibrinogen-positive microthromboemboli (SAH: 9 ± 2; controls: 2 ± 1; P = 0.03) in the hippocampus after aneurysmal SAH. Conclusions. We found clear evidence of early microclot formation in a rabbit model of acute SAH. The extent of microthrombosis did not correlate with early apoptosis or CPP depletion after SAH; however, the total number of TUNEL positive cells in the cortex and the hippocampus significantly correlated with mean CPP reduction during the phase of maximum depletion after SAH induction. Both microthrombosis and neuronal apoptosis may contribute to EBI and subsequent DCI.
Published Version: doi:10.1155/2014/161702
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4109416/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:12785938
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