Page 553

Karger_ESC London_2013

London, United Kingdom 2013 Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 553 499 Translational stroke research Usefulness of circulating apoptotic bodies determination in the prognosis of stroke I. Díaz-Maroto1, J. Garcia-Garcia2, E. Fernández-Díaz3, E. Palazón4, G. Serrano5, O. Ayo-Martín6, T. Segura7 Complejo Hospitalario Universitario de Albacete, Albacete, SPAIN1, Complejo Hospitalario Universitario de Albacete, Albacete, SPAIN2, Complejo Hospitalario Universitario de Albacete, Albacete, SPAIN3, Complejo Hospitalario Universitario de Albacete, Albacete, SPAIN4, Complejo Hospitalario Universitario de Albacete, Albacete, SPAIN5, Complejo Hospitalario Universitario de Albacete, Albacete, SPAIN6, Complejo Hospitalario Universitario de Albacete, Albacete, SPAIN7 Background Apoptosis may play an important role in neuronal death associated with cerebral ischemia. Histo-pathological markers of apoptosis are difficult to obtain in vivo. However, apoptotic bodies (AB) are produced during apoptosis and levels can be measured in peripheral blood samples. Our aim was to assess the possible correlation between circulating levels of AB and clinical out-come in stroke patients. Methods We studied 14 patients with acute ischemic stroke of less than 9 hours of evolution. Serial CA blood determinations and clinical monitoring by NIHSS scale were performed at baseline and 24, 48, 72 and 96 hours after the stroke onset. Stroke etiology by TOAST classification was performed. Results Mean age of 67 yo (4 males and 10 females). Etiologies were: cardioembolic stroke 7 patients, ath-eroembolic stroke 1, lacunar stroke 2 and indeterminated stroke 4. Intravenous thrombolytic treat-ment was administered in 5 patients. Circulating AB levels were detected in all cases. The most sig-nificant variation in the levels of AB was observed comparing the measurement obtained at 24 and 96 hours. In those patients with good clinical outcome (improvement of >3 points in NIHSS scale, n = 6), AB levels lowered at least 50%, except in the patients with lacunar stroke in which AB levels remained unchanged. In those patients with progressive stroke (worsening of >3 points in NIHSS scale, n = 2), AB levels significantly increased ( 40% and 60% in this 2 patients). Conclusion Our results suggest that variations in circulating levels of AB may be a useful marker of progression and / or regression in acute ischemic stroke. 500 Translational stroke research OXALOACETATE INDUCES A POTENTIATION OF THE PROTECTIVE EFFECTS OF GLUTAMATE OXALOACETATE TRANSAMINASE AFTER CEREBRAL ISCHEMIA. M. Pérez-Mato1, P. Ramos-Cabrer2, R. Andrade3, D. Mirelman4, J. Castillo5, F. Campos6 Department of Neurology, Clinical Neurosciences Research Laboratory, Hospital Clínico Uni-versitario, IDIS., Santiago de Compostela, SPAIN1, Department of Neurology, Clinical Neurosci-ences Research Laboratory, Hospital Clínico Universitario, IDIS., Santiago de Compostela, SPAIN2, Department of Neurology, Clinical Neurosciences Research Laboratory, Hospital Clínico Universi-tario, IDIS., Santiago de Compostela, SPAIN3, Department of Biological Chemistry, Weizmann In-stitute of Science., Rehovot, ISRAEL4, Department of Neurology, Clinical Neurosciences Research Laboratory, Hospital Clínico Universitario, IDIS., Santiago de Compostela, SPAIN5, Department of Neurology, Clinical Neurosciences Research Laboratory, Hospital Clínico Universitario, IDIS., San-tiago de Compostela, SPAIN6 Background: The concept of blood glutamate scavenging is increasingly important as a novel and attractive neuroprotectant strategy to reduce the excitotoxic effect of extracellular glutamate during ischemic brain injury. Glutamate-oxaloacetate transaminase (GOT) activation by means of exoge-nous administration of oxaloacetate has been used as the most common protocol to reduce the blood glutamate concentration, however the protective effect of other strategies like recombinant GOT ad-ministration or rGOT supplemented with oxaloacetate have not been tested. So, our aim was to test the protective effect of the administration of rGOT alone and in combination with oxaloacetate in a ischemic model and compare their effects with a oxaloacetate. Methods: Sixty six animals were subjected to a transient middle cerebral artery. Infarct volumes were assessed by magnetic resonance imaging (MRI) before treatment administration, and 24h and 7 days after ischemia. Brain glutamate levels were determined by in vivo MR spectroscopy (MRS) during artery occlusion (80 min) and reperfusion (180 min). Blood and GOT activity was analyzed during occlusion and reperfusion period. Somatosensory test was performed in basal conditions and 7 day after ischemia. Results: In this study we show that, similar than oxaloacetate, administration of rGOT induces a significant reduction of blood and brain glutamate levels which appears reflected in a reduction of infarct volume and sensorimotor deficit after ischemia. However this neuroprotective effect is in-creased when rGOT was administered in combination with a low dose of oxaloacetate. Importantly, the neuroprotective effects of rGOT supplemented with oxaloacetate remain when they were admin-istered also 1 hour after reperfusion. Conclusion: Oxaloacetate induces a potentiation of the protective effects of rGOT after ischemia. The robust protection shown by both compounds suggests it is a strong candidate for a successful acute phase stroke treatment.


Karger_ESC London_2013
To see the actual publication please follow the link above