Minami N, Tani E, Maeda Y, Yamaura I, Nakano A
Department of Neurosurgery, Hyogo College of Medicine, Japan.
Neurosurgery. 1993 Oct;33(4):698-705; discussion 705-6. doi: 10.1227/00006123-199310000-00021.
Vasospasm was produced in the canine basilar arteries by a two-hemorrhage method, and voltage- and receptor-dependent contractions of the normal canine basilar arteries were induced by local applications of potassium chloride (KCI) and serotonin, respectively, after transclival exposure. Actin, myosin, desmin, filamin, talin, vinculin, and alpha-actinin in the basilar artery were studied by immunoblotting. The immunoblots showed a decrease or loss in immunoreactivity of some native proteins and generation of protein fragments, smaller in size than native proteins, in spastic, KCI, and serotonin groups, indicating a proteolytic degradation. In the spastic group on Day 2, actin, desmin, and filamin were usually degraded slightly; myosin moderately; and talin and alpha-actinin substantially. Vinculin and metavinculin remained intact. In the spastic group on Day 7, actin and desmin were usually decomposed slightly; myosin, filamin, and vinculin substantially; and talin, metavinculin, and alpha-actinin markedly. In the KCI and serotonin groups, slight degradation was usually observed in filamin, often in alpha-actinin, and occasionally in actin, whereas desmin, vinculin, and metavinculin were not degraded. In addition, myosin was usually degraded moderately in the KCI group and slightly in the serotonin group, and talin was generally decomposed slightly in the KCI group and moderately in the serotonin group. The degraded fragments, although variable in number and immunoreactivity, were similar in size in the three groups. We suggest that the intracellular devices responsible for contraction of the basilar arteries are degraded more severely in the spastic group than in the KCI or serotonin group, probably by similar proteolytic mechanism and progressively with the passage of time after subarachnoid hemorrhage in vasospasm.
采用两次出血法在犬基底动脉中诱导血管痉挛，经经斜坡暴露后，分别通过局部应用氯化钾（KCl）和血清素诱导正常犬基底动脉的电压依赖性和受体依赖性收缩。通过免疫印迹法研究基底动脉中的肌动蛋白、肌球蛋白、结蛋白、细丝蛋白、踝蛋白、纽蛋白和α - 辅肌动蛋白。免疫印迹显示，在痉挛组、KCl组和血清素组中，一些天然蛋白的免疫反应性降低或丧失，并且产生了比天然蛋白尺寸更小的蛋白片段，表明存在蛋白水解降解。在第2天的痉挛组中，肌动蛋白、结蛋白和细丝蛋白通常轻度降解；肌球蛋白中度降解；踝蛋白和α - 辅肌动蛋白大量降解。纽蛋白和间纽蛋白保持完整。在第7天的痉挛组中，肌动蛋白和结蛋白通常轻度分解；肌球蛋白、细丝蛋白和纽蛋白大量分解；踝蛋白、间纽蛋白和α - 辅肌动蛋白明显分解。在KCl组和血清素组中，通常观察到细丝蛋白轻度降解，α - 辅肌动蛋白常出现降解，肌动蛋白偶尔降解，而结蛋白、纽蛋白和间纽蛋白未降解。此外，在KCl组中肌球蛋白通常中度降解，在血清素组中轻度降解，在KCl组中踝蛋白一般轻度分解，在血清素组中中度分解。尽管降解片段的数量和免疫反应性各不相同，但三组中其大小相似。我们认为，在血管痉挛时，蛛网膜下腔出血后，负责基底动脉收缩的细胞内装置在痉挛组中比在KCl组或血清素组中降解更严重，可能是通过类似的蛋白水解机制，并且随着时间的推移逐渐加重。
