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Address correspondence to Lin Wang or Ji-Xin Shi, Department of Neurosurgery, Jinling Hospital, 305 East Zhongshan Road, Nanjing 210002, P.R. China; tel 86 25 8596 2075; fax 86 25 8480 6839; e-mail wanglin_77{at}hotmail.com.
Subarachnoid hemorrhage (SAH) has considerable mortality and morbidity, but the pathophysiologic mechanism is not entirely clear. Following SAH, blood or its lysate enters the subarachnoid space. This study examined how blood lysate influences the vulnerable brain following SAH. Heparinized hemolysate was slowly injected into the cisterna magna of 10 female rabbits, while a control group of 10 rabbits received a similar injection of heparinized isotonic sodium chloride solution without hemolysate. The basilar artery and brain tissue were excised after perfusion fixation. The degree of cerebral vasospasm was evaluated by measuring the cross-sectional area of the basilar artery, and brain damage was investigated by TUNEL staining. In the SAH group, the apoptosis index of neuronal cells located at the base of the temporal lobe averaged 26% (range = 3 to 56%), which was significantly higher than the corresponding apoptosis index in the control group (mean 0.5%, range = 0 to 4%, p <0.001). The mean cross-sectional area of the basilar artery in the SAH group did not differ significantly from that in the control group. These results suggest that SAH induces apoptosis of neuronal cells by a mechanism that is independent of cerebral vasospasm.
Keywords: subarachnoid hemorrhage, brain damage, apoptosis, basilar artery, cerebral vasospasm
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