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2 Acta Neurobiologiae Experimentalis

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Plasma homocysteine level and the course of ischemic stroke

100%

Pniewski J. , Chodakowska-Zebrowska M. , Wozniak R. , Stepien K. , Stafiej A.

Acta Neurobiologiae Experimentalis

2003

tom 63

nr 2

127-130

Increased level of homocysteine (Hcy) in blood seems to influence negatively the course of ischemic stroke (IS), the possible mechanism of this action could be acceleration of oxidative stress. The aim of this study is to assess the influence of Hcy level in patients with IS on the prognosis 3 moths after the stroke onset. 75 patients aged 68.27 12.62 years, with the diagnosis of first ever IS were examined. Patients with the symptoms corresponding with TACS at the beginning of stroke and with diminished level of consciousness were not included. The level of Hcy over 15 mol/l was assessed as mild hiperhomocysteinemia (MHcy). 74 (98.7%) patients were assessed 3 months after IS onset in the Rankin scale. Recovery was assessed, according to Rankin Scale: good recovery (GR) 0-2, bad recovery (BR) 3-5 and death. MHcy was seen in 9 (14.5%) with GR and in 8 (66.7%) with BR (P=0,0005). MHcy increases the risk of BR 11.78 times (95%CI 2.93-47.42).

NMDA receptors and nitric oxide regulate prostaglandin D2 synthesis in the rabbit hippocampus in vivo

72%

Lazarewicz J. W. , Salinska S. E. , Salinska E. , Stafiej S. A. , Stafiej A. , Ziembowicz Z. A. , Ziembowicz A. , Zieminska Z. E. , Zieminska E.

Acta Neurobiologiae Experimentalis

2000

tom 60

nr 4

427-435

The aim of this in vivo microdialysis study was to characterise the regulation of prostaglandin D2 (PgD2) synthesis by NMDA receptors in the rabbit hippocampus in relation to changes in extracellular Ca2+ concentration ([Ca2+]e) and nitric oxide (NO) levels. Samples of dialysate were analysed for changes in PgD2 concentration, in [Ca2+]e and in the level of NO. The results demonstrated that a 20-min pulse application of 0.1 - 2.5 mM NMDA via a microdialysis probe induced a prolonged stimulation of PgD2 release that was sensitive to competitive NMDA receptor antagonists. An inhibitor of voltage-sensitive Na+ channels, tetrodotoxin, did not influence this effect but significantly suppressed basal PgD2 production, whereas a NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), prevented NMDA-evoked NO release and inhibited NMDA-induced PgD2 release in an L-arginine-sensitive manner. NO donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside, stimulated PgD2 release. NMDA-evoked decrease in [Ca2+]e was insensitive to TTX and L-NAME. These results demonstrate an in vivo NMDA receptor-mediated modulation of PgD2 synthesis in the brain, in which NO participates.