Harada T, Suzuki Y, Satoh S, Ikegaki I, Asano T, Shibuya M, Sugita K
Department of Neurosurgery, Nagoya University School of Medicine, Japan.
Neurosurgery. 1990 Aug;27(2):252-5; discussion 255-6. doi: 10.1097/00006123-199008000-00014.
The role of blood components in cerebral vasospasm was evaluated using an in vivo canine model. An intracisternal injection of 5 ml of washed red blood cells (RBCs) and platelet-rich plasma (PRP) resulted in acute vasospasm of the basilar artery as seen by angiography. This was comparable with the degree of vasospasm induced by an injection of the same amount of whole blood. Repeated injections of blood components or whole blood on Days 1 and 3 induced chronic vasospasm, as shown by angiography on Day 7. Results clearly indicate that chronic vasospasm was produced by RBCs and PRP, and it was in a dose-dependent manner with increasing concentrations of RBCs (hematocrit: 30, 50, and 70%). The vasospasm induced by both components closely reproduced that seen with whole blood. Neither acute nor chronic vasospasm induced by blood component injection was associated with clot formation in the subarachnoid space, as confirmed by an autopsy. These results suggest that the extravasation of RBCs and PRP into the subarachnoid space produces cerebral vasospasm by mechanisms independent of blood clot formation.
使用体内犬模型评估了血液成分在脑血管痉挛中的作用。通过血管造影可见，脑池内注射5毫升洗涤红细胞（RBC）和富含血小板血浆（PRP）会导致基底动脉急性血管痉挛。这与注射相同量全血所诱导的血管痉挛程度相当。在第1天和第3天重复注射血液成分或全血会诱导慢性血管痉挛，如第7天血管造影所示。结果清楚地表明，慢性血管痉挛是由RBC和PRP产生的，并且随着RBC浓度增加（血细胞比容：30%、50%和70%）呈剂量依赖性。两种成分诱导的血管痉挛与全血所见的血管痉挛非常相似。尸检证实，血液成分注射诱导的急性或慢性血管痉挛均与蛛网膜下腔血栓形成无关。这些结果表明，RBC和PRP渗入蛛网膜下腔通过独立于血栓形成的机制产生脑血管痉挛。
