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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
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Haemoglobin scavenging after subarachnoid haemorrhage
A Durnford1, J Dunbar, J Galea
1Clinical Neurosciences, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, UK, andrew.durnford@uhs.nhs.uk.
Acta Neurochirurgica. Supplement
|November 5, 2014
Summary
Clearance of cell-free hemoglobin after subarachnoid hemorrhage (SAH) is crucial. Macrophage scavenger receptor CD163 becomes saturated, impairing hemoglobin clearance and suggesting ADAM17 inhibition as a therapeutic target.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Cell-free hemoglobin clearance is vital post-subarachnoid hemorrhage (SAH) to mitigate vasospasm and neurotoxicity.
- Haptoglobin binds hemoglobin, and macrophages expressing CD163 clear this complex.
Purpose of the Study:
- To investigate the kinetics of hemoglobin and haptoglobin in cerebrospinal fluid following SAH.
- To explore the role of CD163 in hemoglobin clearance and its potential as a therapeutic target.
Main Methods:
- Analysis of hemoglobin and haptoglobin levels in cerebrospinal fluid after SAH.
- Preliminary neuropathological study assessing meningeal CD163 expression.
Main Results:
- Hemoglobin levels increase gradually post-SAH, while haptoglobin rises acutely due to blood injection.
- Haptoglobin levels decline but then rise again, indicating CD163 saturation.
- Meningeal CD163 expression is upregulated, but CD163 is lost in areas with overlying blood.
Conclusions:
- CD163-mediated clearance of hemoglobin-haptoglobin complexes becomes saturated after SAH.
- Loss of CD163 in blood-covered areas suggests impaired clearance.
- Inhibition of ADAM17, the enzyme shedding CD163, may offer a therapeutic strategy for SAH.
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