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Cerebral Immunohistochemical Characterization of the H2S and the Oxytocin Systems in a Porcine Model of Acute Subdural Hematoma.

Authors :
Denoix, Nicole
Merz, Tamara
Unmuth, Sarah
Hoffmann, Andrea
Nespoli, Ester
Scheuerle, Angelika
Huber-Lang, Markus
Gündel, Harald
Waller, Christiane
Radermacher, Peter
McCook, Oscar
Source :
Frontiers in Neurology; 7/7/2020, Vol. 11, p1-12, 12p
Publication Year :
2020

Abstract

The hydrogen sulfide (H<subscript>2</subscript>S) and the oxytocin/oxytocin receptor (OT/OTR) systems interact in trauma and are implicated in vascular protection and regulation of fluid homeostasis. Acute brain injury is associated with pressure-induced edema formation, blood brain barrier disruption, and neuro-inflammation. The similarities in brain anatomy: size, gyrencephalic organization, skull structure, may render the pig a highly relevant model for translational medicine. Cerebral biomarkers for pigs for pathophysiological changes and neuro-inflammation are limited. The current study aims to characterize the localization of OT/OTR and the endogenous H<subscript>2</subscript>S producing enzymes together with relevant neuro-inflammatory markers on available porcine brain tissue from an acute subdural hematoma (ASDH) model. In a recent pilot study, anesthetized pigs underwent ASDH by injection of 20 mL of autologous blood above the left parietal cortex and were resuscitated with neuro-intensive care measures. After 54 h of intensive care, the animals were sacrificed, the brain was removed and analyzed via immunohistochemistry. The endogenous H<subscript>2</subscript>S producing enzymes cystathionine-ɤ-lyase (CSE) and cystathionine-β-synthase (CBS), the OTR, and OT were localized in neurons, vasculature and parenchyma at the base of sulci, where pressure-induced injury leads to maximal stress in the gyrencephalic brain. The pathophysiological changes in response to brain injury in humans and pigs, we show here, are comparable. We additionally identified modulators of brain injury to further characterize the pathophysiology of ASDH and which may indicate future therapeutic approaches. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
16642295
Volume :
11
Database :
Complementary Index
Journal :
Frontiers in Neurology
Publication Type :
Academic Journal
Accession number :
144461036
Full Text :
https://doi.org/10.3389/fneur.2020.00649