Preventive Effects of Intracisternal Alphatochopherol on Cerebral Vasospasm in Experimental Subarachnoid Hamorrhage.
10.3349/ymj.2003.44.6.955
- Author:
Serdar KEMALOGLU
1
;
Umit OZKAN
;
Fahri YILMAZ
;
Erdem AK
;
Hamit ACEMOGLU
;
Gonul OLMEZ
;
Ramazan SIMSEK
;
Abdurrahman BAKIR
Author Information
1. Department of Neurosurgery, School of Medicine, Dicle University, Diyarbakir, Turkey. mserdarkemaloglu@yahoo. com
- Publication Type:Original Article
- Keywords:
Subarachnoid haemorrhage;
cerebral vasospasm;
Vitamin E;
rat
- MeSH:
Animals;
Antioxidants/*administration & dosage;
Injections, Intraventricular;
Male;
Rats;
Rats, Sprague-Dawley;
Subarachnoid Hemorrhage/*complications;
Vasospasm, Intracranial/*etiology/*physiopathology;
alpha-Tocopherol/*administration & dosage
- From:Yonsei Medical Journal
2003;44(6):955-960
- CountryRepublic of Korea
- Language:English
-
Abstract:
Vasospasm is an important cause of morbidity and/or mortality with a subarachnoid haemorrhage (SAH). The roles of lipid peroxidation in a vasospasm caused by a SAH remain to be investigated. The effect of an intracisternal administration of alphatochopherol on a cerebral vasospasm was investigated in an experimental model. The authors assessed whether the administration of alphatochopherol reduced the vasospasm. By means of an intracisternal blood injection model, a SAH was induced in 30 rats, which were randomly divided into three groups, as follows: group I (G1), without a SAH and drug, group II (G2), a SAH alone, group III (G3), a SAH and alphatochopherol. Following the withdrawal of cerebrospinal fluid (CSF), a fresh unheparinized arterial blood was injected into the cisterna magna to induce a SAH. In G3, 20 U (0.4ml) alphatochopherol was intracisternally injected forty-five hours after induction of the SAH. All rats were sacrificed 72 hours after the induction. The basilar artery, with surrounding tissue, was removed from the cranium. The cross-sectional diameter of the lumen and vessel wall of the rat basilar artery was assessed from a planimetric analysis, and changes compared with G1 and G2. The reduction in the luminal cross-sectional diameter of the vessels exposed to subarachnoid blood was found to be 29.01 % (p=0.001). The group treated with alphatochopherol had a 9% reduction (p=0.004). The role of lipid peroxidation on a vasospasm caused by SAH is well known to be critical. Data from the present study indicated that antioxidant therapy, with topical alphatochopherol, may be promising on a vasospasm caused by a SAH.
