Mori T, Nagata K, Matsui T, Ishida T, Ohami H, Asano T
Division of Pathology, Nippon Medical School, Kanagawa, Japan.
Neuropathol Appl Neurobiol. 1995 Oct;21(5):378-85. doi: 10.1111/j.1365-2990.1995.tb01074.x.
We have recently reported that sustained contraction of the canine basilar artery induced by the intrathecal injection of talc (crystallized hydrous magnesium silicate) mimicked delayed vasospasm following subarachnoid haemorrhage. The present study aims to examine the pathomechanism underlying talc-induced vasocontraction, from the viewpoint of free radical theory, which has been established as a cause of delayed vasospasm. We estimated the effects of a prolonged intrathecal infusion of human recombinant Cu/Zn superoxide dismutase (hr SOD) on the contraction of the basilar artery caused by the intrathecal injection of talc in beagle dogs, which were assigned to the three groups: G1, sham operation with saline treatment; G2, talc injection with saline treatment; and G3, talc injection with 2 ml of hr SOD (7 x 10(4) U/ml) treatment. Talc administration resulted in the reduction in the angiographic calibre of the basilar artery by 63 and 61% on days 3 and 7 (G2). The treatment with hr SOD (G3) led to a significant attenuation of talc-induced contraction of the basilar artery on days 3 (P < 0.05 vs. G2) and 7 (P < 0.05 vs. G2). In the basilar artery wall of days 3 and 7 in G2, pathological changes such as myonecrosis, cytoplasmic vacuolation and detached intercellular junctions were observed. However, these pathological changes almost disappeared in G3. The present findings suggest that superoxide anions may initiate and/or mediate talc-induced vasocontraction and subsequent structural damage of the basilar artery.
我们最近报道，鞘内注射滑石粉（结晶水合硅酸镁）诱导犬基底动脉持续收缩，模拟了蛛网膜下腔出血后的迟发性血管痉挛。本研究旨在从自由基理论的角度研究滑石粉诱导血管收缩的发病机制，自由基理论已被确认为迟发性血管痉挛的一个原因。我们评估了在比格犬中鞘内长期输注人重组铜/锌超氧化物歧化酶（hr SOD）对鞘内注射滑石粉引起的基底动脉收缩的影响，将犬分为三组：G1，生理盐水治疗的假手术组；G2，滑石粉注射加生理盐水治疗组；G3，滑石粉注射加2 ml hr SOD（7×10⁴ U/ml）治疗组。滑石粉给药导致第3天和第7天基底动脉血管造影管径分别减少63%和61%（G2组）。hr SOD治疗（G3组）导致第3天（与G2组相比，P<0.05）和第7天（与G2组相比，P<0.05）滑石粉诱导的基底动脉收缩显著减轻。在G2组第3天和第7天的基底动脉壁中，观察到诸如肌坏死、细胞质空泡化和细胞间连接分离等病理变化。然而，这些病理变化在G3组几乎消失。目前的研究结果表明，超氧阴离子可能引发和/或介导滑石粉诱导的血管收缩以及随后基底动脉的结构损伤。
