The role of microclot formation in an acute subarachnoid hemorrhage model in the rabbit

Andereggen, Lukas; Neuschmelting, Volker; von Gunten, Michael; Widmer, Hans Rudolf; Fandino, Javier; Marbacher, Serge (2014). The role of microclot formation in an acute subarachnoid hemorrhage model in the rabbit. BioMed research international, 2014, p. 161702. Hindawi Publishing Corporation 10.1155/2014/161702

[img]
Preview
Text
the role of microclot formation in an acute subaranoid hemorrhage model in the rabbit.pdf - Published Version
Available under License Creative Commons: Attribution (CC-BY).

Download (2MB) | Preview

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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Intensive Care, Emergency Medicine and Anaesthesiology (DINA) > Clinic of Intensive Care
04 Faculty of Medicine > Service Sector > Institute of Pathology
04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurosurgery
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > Forschungsbereich Mu50 > Forschungsgruppe Neurochirurgie

UniBE Contributor:

Andereggen, Lukas, Widmer, Hans Rudolf

Subjects:

600 Technology > 610 Medicine & health

ISSN:

2314-6133

Publisher:

Hindawi Publishing Corporation

Language:

English

Submitter:

Nicole Söll

Date Deposited:

16 Mar 2015 16:12

Last Modified:

05 Dec 2022 14:43

Publisher DOI:

10.1155/2014/161702

PubMed ID:

25110658

BORIS DOI:

10.7892/boris.65150

URI:

https://boris.unibe.ch/id/eprint/65150

Actions (login required)

Edit item Edit item
Provide Feedback