Document Detail


Lamotrigine attenuates cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.
MedLine Citation:
PMID:  18291450     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Increasing evidence implicates voltage-dependent sodium and potassium channels, in addition to calcium channels of various types, in the pathophysiological development of cerebral vasospasm. This study investigated the ability of LTG, an antiepileptic drug with multi-ion channel inhibition properties, to prevent cerebral vasospasm and subsequent neural ischemia in a rabbit model of SAH. METHODS: Thirty-five New Zealand white rabbits were assigned to 1 of 3 groups: (1) control (no SAH, saline injection); (2) SAH alone; (3) SAH + LTG, 20 mg/kg daily. Animals were killed 72 hours after SAH, then basilar artery lumen areas and arterial wall thickness were measured in all groups. The histological sections of the CA1 and CA3 regions and dentate gyri of the hippocampi were evaluated semiquantitatively for neural tissue degeneration. RESULTS: In the SAH group, the mean luminal cross-sectional area of the basilar artery was reduced by 62% after SAH as compared with the non-SAH controls (P < .0001). After SAH, the vasospastic response was attenuated by 36% in animals treated with 20 mg/kg of LTG compared with the SAH group (P < .005). The mean luminal cross-sectional areas of the basilar artery were 279000 +/- 27000 microm(2) in the control group, 173000 +/- 17600 microm(2) in the SAH group, and 236000 +/- 10000 microm(2) in the SAH + LTG group. The differences between the SAH group and the LTG-treated group were statistically significant (P < .0001). Histological examination was done in 12 control, 12 SAH, and 9 SAH + LTG-treated animals. The mean degeneration score for the control group and SAH + LTG group was statistically significant (P = .012). The difference between the SAH group and SAH+ LTG group was also statistically significant (P = .006). CONCLUSIONS: These findings demonstrate that oral administration of LTG has marked neuroprotective effect and significantly attenuates cerebral vasospasm after SAH, thus providing additional support for the role of non-L-type calcium channels and voltage-dependent sodium channels in vasospasm.
Authors:
Hakan Seçkin; Kazim Yigitkanli; Omer Besalti; Kemal Kosemehmetoglu; Evrim Ozturk; Serkan Simsek; Deniz Belen; Murad Bavbek
Publication Detail:
Type:  Journal Article     Date:  2008-03-04
Journal Detail:
Title:  Surgical neurology     Volume:  70     ISSN:  0090-3019     ISO Abbreviation:  Surg Neurol     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-09-16     Completed Date:  2008-11-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0367070     Medline TA:  Surg Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  344-51; discussion 351     Citation Subset:  IM    
Affiliation:
Ministry of Health, Diskapi Training and Research Hospital, Ankara, Turkey. doktorkazim@mynet.com
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MeSH Terms
Descriptor/Qualifier:
Animals
Basilar Artery / pathology
Calcium Channels / physiology
Disease Models, Animal
Excitatory Amino Acid Antagonists / pharmacology*
Hippocampus / pathology
Male
Rabbits
Severity of Illness Index
Subarachnoid Hemorrhage / drug therapy*,  pathology
Triazines / pharmacology*
Vasospasm, Intracranial / drug therapy*,  pathology
Vertebrobasilar Insufficiency / drug therapy*,  pathology
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Excitatory Amino Acid Antagonists; 0/Triazines; 84057-84-1/lamotrigine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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