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Indexed/Abstracted in: e-psyche, EMBASE, PubMed/MEDLINE, Neuroscience Citation Index, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,651
Online ISSN 1827-1855
Altintas O. 1, Antar V. 2, Baran O. 2, Karatas E. 3, Altintas M. O. 4, Kesgin S. 3, Buyukpinarbasili N. 5, Kocyigit A. 3, Asil T. 6
1 Bor State Hospital, Department of Neurology, Bor/ Nigde /Turkey;
2 Istanbul Training and Research Hospital, Department of Neurosurgery, Kasap İlyas District. Org. Abdurrahman Nafiz, Istanbul, Turkey;
3 Bezmi Alem Vakıf University, Medical Faculty, Department of Biochemistry, Adnan Menderes Bulvarı, Fatih, Istanbul, Turkey;
4 Fatih University, Department of Genetic and Bioengineering, Buyukcekmece Campus, Buyukcekmece/İstanbul;
5 Bezmi Alem Vakıf University, Medical Faculty, Department of Pathology, Adnan Menderes Bulvarı, Fatih, Istanbul, Turkey;
6 Bezmi Alem Vakıf University, Medical Faculty, Department of Neurology, Adnan Menderes Bulvarı, Fatih, Istanbul, Turkey
INTRODUCTION: Despite optimal medical therapy the mortality rate approaches 50% in MCA infarctions. Although recent studies have been showed life-saving effect of hemicraniectomy; there are a few data available in regard to neuroprotection effect of decompressive craniectomy (DC). We induced a malign cerebral ischemia model by intraluminal permanent middle cerebral artery occlusion (MCAo) in male rats for defining the neuroprotective effects of early DC on brain-blood barrier (BBB) molecular changes, infarct size and cerebral edema.
MATERIAL-METHOD: 48 male Spraque Dawley rats were allocated to 4 groups; sham (n = 9), control (n = 9), experiment 1 (n = 15), experiment 2 (n = 15). DC was performed by creating a bone flap, after MCAo at 4th and 24th hours. After 28 hours of survival, all animals were sacrificed. Infarction volumes were calculated from TTC (2,3,5,triphenyltetrozolium chloride)- stained brain sections. In all groups, cerebral edema was quantified as a change in the percentage (%) of brain water content. Western Blot was used to analyze the expression of tight junction protein claudin-5 and occludin.
RESULTS: Brain water content was calculated 75,18±0,75 % in the early DC group and 77,76 ± 0,71 % in the late DC group. No significant difference was found between experiment groups (p= .178). In the early DC group; occludin and claudin-5 were significantly expressed at higher levels compared to late DC group (for occludin p = .013; for claudin-5 p = .034). At early DC group (73,38±23,11 mm3) the final infarct volumes (in terms of cubic millimeters; mm3) were significantly smaller than in the late DC group (377,18±39,23 mm3) (p = .013).
CONCLUSION: The study results supported the neuroprotective effects of early DC in malign MCA infarcts.