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.
Animals ; Antioxidants/*administration & dosage ; Injections, Intraventricular ; Male ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage/*complications ; Vasospasm, Intracranial/*etiology/*physiopathology ; alpha-Tocopherol/*administration & dosage

OBJECTIVETo discuss the mechanism of cerebral vessel spasm caused by concussion and the effect of Nimodipine on concussion.

METHODSA total of 224 patients who were treated from March 1995 to October 1999 were divided into two groups randomly, ie, Nimodipine group (113 cases) and control group (111 cases). Middle cerebral artery (MCA), basilar artery (BA) and the average peak forward velocity of cerebral blood flow were observed by color three-dimensional transcranial Doppler (3D-TCD) within 24 hours after admission and at the end of 3-6 days of treatment. Cerebral blood flow changes, characteristics and treatment effect were analyzed and determined by clinical main symptom disappearance rate.

RESULTSIn concussion, cerebral blood flow was divided into 3 phases: cerebral blood flow low infusion dilation phase, cerebral blood vessel spasm phase and cerebral blood flow recovery phase. In the Nimodipine group, clinical main symptom disappearance rate was higher than that in the control group in the cerebral spasm and recovery phases with a significant difference (P < 0.01).

CONCLUSIONSCerebral vessel spasm, hypoxia and ischemia lesion are the main pathological changes. Whether cerebral dysfunction is reversible or not is mainly determined by spasm time of cerebral blood vessel. Nimodipine has a good effect on releasing spasm and diminishing the cerebral blood flow velocity. It not only improves curative effect on concussion, but also reduces and prevents concussion sequelae. Hence, concussion patients who have cerebral spasm confirmed by 3D-TCD should be given Nimodipine routinely and early.

Adolescent ; Adult ; Aged ; Blood Flow Velocity ; Brain Concussion ; complications ; diagnostic imaging ; Cerebral Arteries ; diagnostic imaging ; drug effects ; Cerebrovascular Circulation ; drug effects ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Drug Therapy, Combination ; Female ; Follow-Up Studies ; Humans ; Infusions, Intravenous ; Injury Severity Score ; Male ; Mannitol ; administration & dosage ; Middle Aged ; Nimodipine ; administration & dosage ; Reference Values ; Treatment Outcome ; Ultrasonography, Doppler, Transcranial ; Vasospasm, Intracranial ; drug therapy ; etiology ; physiopathology