Peerless S J, Fox A J, Komatsu K, Hunter I G
Stroke. 1982 Jul-Aug;13(4):473-9. doi: 10.1161/01.str.13.4.473.
A model for producing chronic cerebral vasospasm in monkeys by injecting autologous blood into the basal cistern is described. Spasm/narrowing was observed by angiography one hour after SAH in 8 out of 10 monkeys and in 5 of these 8, spasm was observed both one and two weeks later. No narrowing of the vessels was observed in the control cases. In monkeys that showed spasm one week after SAH, narrowing of the extracranial vertebral arteries was also observed. Repeated injections of blood at intervals of one and two weeks caused intensification of spasm in the intracranial portion of vertebral arteries and the basilar arteries. It is suggested that cerebral vasospasm following SAH may in part be mediated by a central control mechanism acting through the sympathetic nervous system in that extracranial vessels remote from direct contact with blood showed reactive narrowing.
描述了一种通过向基底池注射自体血液在猴子中产生慢性脑血管痉挛的模型。10只猴子中有8只在蛛网膜下腔出血(SAH)后1小时通过血管造影观察到痉挛/狭窄,在这8只中的5只中,在1周和2周后均观察到痉挛。在对照病例中未观察到血管狭窄。在SAH后1周出现痉挛的猴子中,还观察到颅外椎动脉狭窄。每隔1周和2周重复注射血液会导致椎动脉颅内部分和基底动脉的痉挛加剧。提示SAH后的脑血管痉挛可能部分由通过交感神经系统起作用的中枢控制机制介导,因为远离与血液直接接触的颅外血管出现了反应性狭窄。