Kaplan B J, Gravenstein N, Friedman W A, Blackmore J A, Day A L
Neurosurgery. 1986 Jul;19(1):41-8. doi: 10.1227/00006123-198607000-00006.
Vasospasm of the vertebrobasilar system was induced in seven dogs by the intracisternal injection of autologous blood. Somatosensory and brain stem auditory evoked potentials were recorded before and after the induction of angiographically confirmed vasospasm. Additionally, somatosensory evoked potentials were monitored during graded hypotension to 40 mm Hg. There was no significant alteration in the evoked potentials by vasospasm or hypotension. Detailed clinical examination and postmortem histopathological studies did not demonstrate any focal neurological deficit or infarction attributable to vasospasm. Previous studies have noted close correlations between decreased cerebral blood flow and evoked potential alterations. Induced hypotension to a mean arterial pressure of 40 mm Hg in the presence of documented vasospasm was not sufficient to cause evoked potential changes, focal neurological deficit, or pathological evidence of infarction in the canine model.
通过向七只狗的脑池内注射自体血液诱导椎基底动脉系统血管痉挛。在血管造影证实血管痉挛诱导前后记录体感和脑干听觉诱发电位。此外，在将血压分级降至40mmHg的过程中监测体感诱发电位。血管痉挛或低血压并未使诱发电位发生显著改变。详细的临床检查和死后组织病理学研究未发现任何可归因于血管痉挛的局灶性神经功能缺损或梗死。先前的研究已经注意到脑血流量减少与诱发电位改变之间存在密切关联。在已证实存在血管痉挛的情况下，将犬模型的平均动脉血压降至40mmHg不足以引起诱发电位变化、局灶性神经功能缺损或梗死的病理证据。
