Poster Abstracts Thursday, November 10, 2005 $423

of statins could be useful for preventing neuronal damage in cerebral ischemia.

1266 Comparison of treahnent outcoule in patients with Stroke adulitled in ICU and Neurologie ward of a hospital in Isfallan

Najafi, M ~, Golshiri, pa, Reissifar M a, Khodabandehloo, R ~, Najafi, F ~. ~Isfahan University of Medical Seienees,Isfahan, Iron.." 2Tehran University of Medical Sciences, Tehran, Iron

Background: Taking care of stroke patients adnritted in Intensive Unit Care (ICU) costs very nmch, in comparison with adnfission in general neurology ward. The goal of this study was assessment of outcome in patients with stroke admitted in ICU in comparison with general neurology ward. Method: We assess 100 patients with moderate or severe stroke according to National Institute of Health Stroke Scale (NIHSS). Outcome treatnrent and the complications of stroke were assessed. The patients were allocated randomly in ICU or general ward and matching was done according to age, sex and NIHSS. Blood pressure, blood glucose, evidences for pulmonary infections, bed sore, mortality and duration of admission were assessed. The results analysed using SPSS software. Results: There was no meaningful different between ICU and ward in the cases of hypertension control, diabetes control or occuring pneumonia and mortality rate (P > 0.05). But incidence of bedsore was significantly different between two wards with the relative risk of 1.5. Also, tire duration of bedridden was significantly different (P< 0.001). Conclusion: Tiffs study shows that there are not significant difference in the cares that are given in the ICU and general neurology ward. Thus, these cost analysis studies will help physicians deciding to admit patients with stroke in different wards. Improvement of cares quality in general wards may be a suitable approach for hospitals to decline extra costs.

1267 The role of Matrix Metalloproteinase-2 in white matter lesions of Chronic Cerebral Hypoperfusion in rodents

Nakaji, K ~, lhara, M a, Tomimoto, H a, Noda M 2, Takahashi, R 1. 2Department of Neurology, Kyoto University Graduate School of Medicine, Japan," 2Department of molecular oncology, Kyoto University Graduate School of Medicine, Japan

Background: Cerebrovascular white matter (WM) lesions are asso- ciated with denrentia in the elderly. Our previous study showed that matrix metalloproteinase (MMP)-2 might contribute to WM lesion formation in a rat model of chronic cerebral hypoperfusion. To further investigate tire role of MMP-2, we evaluate tire effects of M M P inhibitor (AG3340) on the WM lesions in the rat model and the degree of WM lesions induced by hypoperfusion in the MMP-2 null mice. Method: Cerebral hypoperfusion was induced by occlusion of bilateral common carotid arteries in male Wister rats (in - 30) and by stenosis of ffrenr with external microcoils in MMP-2 null mace (n - 20) and their littermate controls (in -- 20). Rats were treated twice a day with AG3340 (100 mg/Kg i.p.) or vehicle from just before the operation to day 14. The Khiver-Barrera stain was used to assess the severity of WM lesions (0, none; 1, mild; 2, moderate; 3, severe). Antibodies against GFAP and lectin were used to evaluate astrocytic gliosis and microglial proliferation imnrunotfistochemically. Blood-brain barrier permeability was examined by extravasation of injected Evans blue. Results: The AG3340 treatment in rats and MMP-2 knockout in mice significantly improved the severity of WM lesions (WM lesion score, 1.3 9- 0.5 vs. 0.5 9- 0.4 in rats; 1.5 9- 0.8 vs. 0.5 9- 0.8 in mice), significantly reduced tire nunrber of astrocytes/activated microglia in tire WM, and eliminated perivascular extravasation of Evans blue as compared with ffreir controls.

Conclusion: Pharmacologic and genetic inhibition of MMP-2 had a protective role in WM lesions in rodents.

1268 Rosuvastafin itfllibits Post-Iseheulic Leukocytes adhesion in Cerebral Venules and Veins

Nakajima, S ~;z, Sawada, S ~, Ognra, M ~, Fukushima, K a, Ohsuzu, F ~, Nomura, S 2. list Internal Medicine, NDMC, Tokorozawa, Japan; 2Neurology/Psychiatry, NDMC, Tokorozawa, Japan

Background: Statins are known to decrease tire stroke morbidity in clinical trials, but tire nature of pleiotropic effects during the acute stroke stage remains to be analyzed. We tried to investigate the direct effect of rosuvastatin, a potent new HMG-CoA reductase inhibitor, against the cerebrovascular inflammation in a murine ischemia- reperfusion model. Method: Closed cranial windows were fixed 24 hours after the 60 minute occlusion of bilateral carotid arteries, and cerebrovascular adhesion of leukocytes stained by rhodamine 6G were counted by the laser scanning microscope in untreated and rosuvastatin-treated C57BL/6J male mice. Rosuvastatin at a dose of 1 mg/kg was administered intraperitoneally for 3 days prior to ischemia. The m R N A level of ICAM-1, VCAM-1, and MCP-1 in the post-ischemic carotid arteries, cerebral cortex, and cerebral veins were measured by the real-time polymerase chain reaction. Results: At 24 hours after ischemia-reperfusion, leukocytes adhesion and transmigration rose markedly in post-capillary venules and veins, and pretreatnrent by rosuvastatin significantly reduced these inflanr- matory changes. The m R N A levels for ICAM-1, VCAM-1, and MCP-1 increased in post-ischemic carotid artery, cortex and vein at 24 hours after the ischemic load. Rosuvastatin pretreatment also reduced the m R N A expression significantly in all three inflammatory factors. Conehision: Rosuvastatin attenuated the cerebrovascular inflammation in tire acute stage after ischenria-reperfusion episode, accompanied by tire significant intfibition of gene expression of adhesion molecules and chemotactic molecule. These data may indicate one of tire pleiotropic effects of the rosuvastarin treatment to improve the outcome in acute stroke cases with ischemia-reperfusion episodes.

1269 C×43 expression and neuroprotection in human isdlemie brain injury

Nakm~e, T 1, Yoshida, ya, Nagata, K a. 2Research Institute for Brain and Blood Vessels, Akita, Japan

Background: Astrocytes establish a glial network and communicate through gap junctions in tire brain. Comrexin 43 (C×43) is one of major component proteins in astrocytic gap junctions. Although astrocytes play a critical role in supporting neurons, the role of astrocytic gap junctions under ischemic condition remains controver- sial. Since most of studies have been performed using animal models, we investigated the C×43 expression in human brain after stroke. We also observed uncoupling proteins (UCP) -2 and 5, which are reported to relate to tire neuronal protection, to determine tire influence of neuroprotection. Methods: Slice sections were prepared from brains which had been taken from pathological samples in our hospital. Embolic stroke brains sectioned within a few days because of the stroke were considered as acute ischemic models. Multiple lacunar infarction brains sectioned because of pneunlonia or cancer were considered as chronic models. We observed the expression level of C×43, UCP-2 and 5 in both lesioned and intact areas, and compared them between acute and chronic models. Results: The C×43 expression was significantly amplified in the lesion of chronic models as compared to acute models. Even in the intact cortex, tire C×43 expression of chronic models was tfigher than that of acute models. UCP-2 expression was significantly increased in the ischemic lesion compared to the intact area. The level of UCP-5