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66th Annual Meeting of the German Society of Neurosurgery (DGNC)
Friendship Meeting with the Italian Society of Neurosurgery (SINch)

German Society of Neurosurgery (DGNC)

7 - 10 June 2015, Karlsruhe

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Effect of Iloprost in the early phase after experimental subarachnoid hemorrhage

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  • Diana Pupke - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Stefan Köhler - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Judith Weiland - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Nadine Willner - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Ralf-Ingo Ernestus - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg
  • Thomas Westermaier - Neurochirurgische Klinik und Poliklinik, Universitätsklinikum Würzburg

Deutsche Gesellschaft für Neurochirurgie. 66. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Karlsruhe, 07.-10.06.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. DocP 148

doi: 10.3205/15dgnc546, urn:nbn:de:0183-15dgnc5467

Published: June 2, 2015

© 2015 Pupke et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

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Objective: Subarachnoid hemorrhage (SAH) is a life threatening disease with a high morbidity and mortality. Mechanisms of early brain injury are not completely understood but reduced cerebral blood flow (CBF) due to elevation of intracranial pressure (ICP) and acute vasospasm seems to play an important role. In this experimental study the effect of the vasodilatator Iloprost, a synthetic Prostaglandin PGI2 analogon, in the acute phase after SAH was investigated.

Method: Subarachnoid hemorrhage was induced by the endovascular filament model in male Sprague dawley rats (n=22). Sham-operated animals underwent an identical procedure without vessel perforation (n=4). Iloprost (1ng/kg BW/h) was continuously administered via jugular vein catheter from 30 to 180 minutes after SAH (n=10). CBF was measured via Laser Doppler Flow monitoring (LDF) over both hemispheres before and in the first three hours after bleeding. ICP, arterial blood pressure, cerebral perfusion pressure (CPP) and body temperature were recorded continuously. Animals were sacrificed at 24 hours following SAH. Extent of SAH and clinical outcome were evaluated using modified grading systems by Sugawara et al. (2008). Immunohistochemical (Caspase 3) and histological (HE) stainings were performed to asses hippocampal damage.

Results: Cerebral blood flow significantly decreased immediately after SAH to a mean level of 23% of baseline (p<0.001). 30 minutes after start of the Iloprost infusion mean LDF values significantly increased compared to the control group (p<0.05) and stayed on a higher level until the end of intervention. Arterial blood pressure did not decrease by application of Iloprost. The clinical outcome was better in the Iloprost group with a significantly better neurological score (p<0.05) and a lower mortality rate (20% vs. 42%). Mean extent of SAH was comparable in both groups. Histological hippocampal damage was increased in control animals.

Conclusions: Our results suggest that application of Iloprost in the acute phase after SAH leads to an increase of cerebral blood flow, possibly by inhibition of acute vasospasm. This may lead to a better clinical outcome in this critical phase after SAH. Blood pressure was not negatively affected by the medication. As Iloprost is a substance already approved for clinical use, it could be a potential therapeutic agent for SAH.