Macdonald R L, Weir B K, Grace M G, Martin T P, Doi M, Cook D A
Division of Neurosurgery, University of Alberta, Edmonton, Canada.
Blood Vessels. 1991;28(6):498-510. doi: 10.1159/000158896.
Whether vasospasm results from smooth muscle contraction or from arterial wall infiltration by cells and other material is subject to debate. Computer-assisted image analysis was used to measure lumen area, total wall area, and area of tunica media plus tunica intima of cross-sections of monkey right middle cerebral arteries (MCAs), exposed in vivo for 6 days to whole blood (n = 4), oxyhemoglobin (OxyHb, n = 5), methemoglobin (MetHb, n = 5), bilirubin (n = 5), mock cerebrospinal fluid (CSF, n = 6), and supernatant fluid from an incubated mixture of autologous blood and mock CSF (n = 5). Five control (left) MCAs from each group and 4 MCAs contracted in vitro with potassium chloride were measured. Significant angiographic vasospasm occurred in groups receiving whole blood, supernatant fluid, and OxyHb (p less than 0.05). There was significant correlation (r = 0.58, p less than 0.05) between right MCA diameter on angiography and diameter calculated from lumen area. When compared to effects of mock CSF, OxyHb significantly increased total wall area. When right and left MCAs were compared within groups, total wall area increased in every group with significant increases in groups exposed to mock CSF, OxyHb, and bilirubin (p less than 0.05). No changes developed in area of tunica media plus tunica intima, whether comparing right versus left MCAs within groups or right MCAs between groups. Contraction in vitro did not significantly increase total wall area or area of tunica media plus tunica intima. Light microscopy demonstrated inflammatory debris in the tunica adventitia of arteries from every group. This study shows that whole blood, OxyHb, and supernatant fluid, which contains OxyHb, cause vasospasm. Increases in total wall area are not sufficient to account for luminal narrowing, and therefore, changes such as cell proliferation and arterial wall fibrosis in the intima or media apparently do not contribute primarily to arterial narrowing of vasospasm but could be related to persistence of narrowing. Vessel wall thickening, which does occur, is caused by increased tunica adventitia area only and is nonspecific in that it develops after injection of substances not associated with vasospasm. The data are consistent with the hypothesis that oxyHb causes vasospasm (both angiographic and morphologic) by inducing muscle contraction in the media.
血管痉挛是由平滑肌收缩引起还是由细胞及其他物质浸润动脉壁所致，目前仍存在争议。采用计算机辅助图像分析技术测量了猴右大脑中动脉（MCA）横截面的管腔面积、总壁面积以及中膜加内膜面积，这些动脉在体内分别暴露于全血（n = 4）、氧合血红蛋白（OxyHb，n = 5）、高铁血红蛋白（MetHb，n = 5）、胆红素（n = 5）、模拟脑脊液（CSF，n = 6）以及自体血与模拟脑脊液孵育混合物的上清液（n = 5）中6天。对每组的5根对照（左）MCA以及4根在体外被氯化钾收缩的MCA进行了测量。接受全血、上清液和OxyHb的组出现了显著的血管造影性血管痉挛（p < 0.05）。血管造影上右MCA直径与根据管腔面积计算出的直径之间存在显著相关性（r = 0.58，p < 0.05）。与模拟脑脊液的作用相比，OxyHb显著增加了总壁面积。当在组内比较左右MCA时，每组的总壁面积均增加，暴露于模拟脑脊液、OxyHb和胆红素的组增加显著（p < 0.05）。无论在组内比较左右MCA还是在组间比较右MCA，中膜加内膜面积均无变化。体外收缩并未显著增加总壁面积或中膜加内膜面积。光学显微镜检查显示每组动脉外膜存在炎性碎屑。本研究表明，全血、OxyHb以及含有OxyHb的上清液可导致血管痉挛。总壁面积的增加不足以解释管腔狭窄，因此，内膜或中膜中的细胞增殖和动脉壁纤维化等变化显然并非血管痉挛性动脉狭窄的主要原因，但可能与狭窄的持续存在有关。确实发生的血管壁增厚仅由外膜面积增加引起，且是非特异性的，因为它在注射与血管痉挛无关的物质后出现。这些数据与以下假设一致，即氧合血红蛋白通过诱导中膜肌肉收缩导致血管痉挛（血管造影和形态学方面）。
