gms | German Medical Science

65th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

11 - 14 May 2014, Dresden

Time course of hemoglobin distribution following subarachnoid hemorrhage

Meeting Abstract

  • Stefan Köhler - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Nadine Willner - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Thomas Westermaier - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Christian Stetter - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Ralf-Ingo Ernestus - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Jin-Yul Lee - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg

Deutsche Gesellschaft für Neurochirurgie. 65. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Dresden, 11.-14.05.2014. Düsseldorf: German Medical Science GMS Publishing House; 2014. DocP 161

doi: 10.3205/14dgnc555, urn:nbn:de:0183-14dgnc5551

Published: May 13, 2014

© 2014 Köhler et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Objective: Aneurysmal subarachnoid hemorrhage (SAH) is a life-threatening disease. The mortality is high within few days following hemorrhage. Although the underlying injury mechanisms are not completely understood, the amount of subarachnoid blood most likely plays an important role regarding clinical outcome. The purpose of this study was to investigate the distribution of subarachnoid hemoglobin in the brain during the first days following SAH.

Method: Sprague-Dawley rats were subjected to subrachnoid hemorrhage using the prechiasmatic injection model (n=28). Biotin-marked hemoglobin (1 mg) was injected into the prechiasmatic cistern. Animals were sacrificed at 3, 6 and 12 h and Day 1, 3 and 7 following hemoglobin injection (n=4, each). In control rats, PBS buffer (pH 7.4) was injected intracisternally (n=4). Hemoglobin distribution was visualized immunohistochemically using streptavidin-horseradish peroxidase. To assess neuro-glial changes additional immunohistochemical stainings for HO-1 expression and detection of apoptotic neuro-glial cells by the TUNEL-method were performed.

Results: Extensive accumulation of hemoglobin was observed not only in the entire subarachnoid space, but also in the basal part as well as in the periventricular region of the ipsilateral brain tissue leading to diverse neuro-glial changes. In regions of hemoglobin accumulation, the number of HO-1- and TUNEL-positive neuro-glial cells was markedly increased.

Conclusions: In addition to global cerebral ischemia in the early phase after SAH, excessive hemoglobin and iron overload cause brain injury by delayed mechanisms. Therefore, early acute treatment with iron chelator might be useful to ameliorate iron-induced secondary brain injury following SAH.