RGD Reference Report - Erythropoietin prevents delayed hemodynamic dysfunction after subarachnoid hemorrhage in a randomized controlled experimental setting. - Rat Genome Database

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Erythropoietin prevents delayed hemodynamic dysfunction after subarachnoid hemorrhage in a randomized controlled experimental setting.

Authors: Guresir, E  Vasiliadis, N  Konczalla, J  Raab, P  Hattingen, E  Seifert, V  Vatter, H 
Citation: Guresir E, etal., J Neurol Sci. 2013 Sep 15;332(1-2):128-35. doi: 10.1016/j.jns.2013.07.004. Epub 2013 Jul 30.
RGD ID: 10400909
Pubmed: PMID:23907045   (View Abstract at PubMed)
DOI: DOI:10.1016/j.jns.2013.07.004   (Journal Full-text)

INTRODUCTION: Erythropoietin (EPO) was proven as a promising approach for experimental subarachnoid hemorrhage (SAH). Clinical data are, however, inconclusive so far. A detailed characterization of specific EPO effects could facilitate the design of trials. The aim of the present investigation was, therefore, to characterize these effects on prevention of delayed proximal cerebral vasospasm (CVS), impaired microcirculation and cerebral blood flow (CBF) after experimental SAH. METHODS: 27 male Sprague-Dawley rats were randomized in 3 groups: Sham, SAH control, and SAH EPO. SAH was induced by injection of 0.2ml autologous blood into the cisterna magna on days 1 and 2. Animals of the SAH EPO group received 5000iU rh EPO alpha 6h after the 2nd SAH intravenously. Surviving animals were examined on day 5 by MR perfusion weighted imaging (PWI). Cerebral blood flow (CBF) and volume (CBV) were determined by PWI, proximal CVS by basilar artery (BA) diameter, and neuroprotection by hippocampal cell count (CA1-CA4). RESULTS: BA diameter was significantly reduced in both SAH groups, but improved significantly after EPO (Sham: 144+/-3mum, SAH control: 79+/-6mum, SAH EPO 109+/-4mum). The rrCBV ratio was 8.78+/-0.72 Sham, 5.14+/-1.73 SAH control, and 6.80+/-0.44 SAH EPO. The improvement by EPO did not reach statistical significance. RrCBF ratio was also significantly reduced in both SAH groups, but was significantly improved by EPO (Sham: 8.78+/-0.34, SAH control: 4.26+/-1.05, SAH EPO 5.85+/-0.46). Surviving neuronal cells were significantly reduced in SAH controls in all areas, but in SAH EPO only in CA1. CONCLUSION: The present data suggest that an EPO application in a timely distance to the SAH is sufficient to prevent delayed proximal CVS, but that the doses were insufficient to improve microcirculation or to be directly neuroprotective.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
EPOHumanSubarachnoid Hemorrhage treatmentIDA  RGD 
EpoRatSubarachnoid Hemorrhage treatmentISOEPO (Homo sapiens) RGD 
EpoMouseSubarachnoid Hemorrhage treatmentISOEPO (Homo sapiens) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Epo  (erythropoietin)

Genes (Mus musculus)
Epo  (erythropoietin)

Genes (Homo sapiens)
EPO  (erythropoietin)


Additional Information