Bulter W E, Peterson J W, Zervas N T, Morgan K G
Neurosurgical Service, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Neurosurgery. 1996 Apr;38(4):781-7; discussion 787-8. doi: 10.1227/00006123-199604000-00029.
It remains unknown what proportion of delayed arterial narrowing after subarachnoid hemorrhage depends on ongoing metabolic activity within arterial smooth muscle cells versus changes in the passive structural properties of the arterial wall. To determine this, vasospasm was induced by the double subarachnoid hemorrhage model. Anterior spinal artery segments were harvested from control dogs and from dogs with vasospasm. The segments were suspended in a force transducer and stretched to an optimal length for contraction. The difference in tension between 37 and 0 degrees C was defined as the intrinsic tone, and the residual tension at 0 degrees C was defined as the passive tension. The segments taken from dogs with vasospasm had increased intrinsic tone and passive tension (the differences were 3.8 kN/m2 [P < 0.05] and 14.8 kN/m2 [P < 0.025], respectively). Hence, the passive component accounted for 79.6% of the increased tension in vasospastic arterial segments. The intracellular calcium concentration was measured in these segments, using the luminescent calcium indicator, aequorin. The vasospastic segments had increased basal intracellular calcium concentration (398 versus 258 nmol/L, P < 0.025). In parallel experiments, control and vasospastic vessels were immediately excised when the animals were killed, and the vessels were quick-frozen. Subsequently, using two-dimensional gel electrophoresis to measure percent myosin light chain phosphorylation, vasospastic vessels were found to have increased myosin light chain phosphorylation (37 versus 2%, P < 0.05). The increased intracellular calcium concentration and increased percent myosin light chain phosphorylation in vasospastic segments implicate a role for the Ca(2+)-dependent pathway of smooth muscle cell contraction in vasospasm.
蛛网膜下腔出血后延迟性动脉狭窄中，有多大比例取决于动脉平滑肌细胞内持续的代谢活动，又有多大比例取决于动脉壁被动结构特性的改变，目前尚不清楚。为了确定这一点，采用双次蛛网膜下腔出血模型诱导血管痉挛。从对照犬和患有血管痉挛的犬身上采集脊髓前动脉节段。将这些节段悬挂在力传感器中，并拉伸至收缩的最佳长度。37℃和0℃时的张力差定义为固有张力，0℃时的残余张力定义为被动张力。取自患有血管痉挛犬的节段固有张力和被动张力均增加（差异分别为3.8 kN/m2 [P < 0.05]和14.8 kN/m2 [P < 0.025]）。因此，被动成分占血管痉挛性动脉节段张力增加的79.6%。使用发光钙指示剂水母发光蛋白测量这些节段中的细胞内钙浓度。血管痉挛节段的基础细胞内钙浓度增加（398对258 nmol/L，P < 0.025）。在平行实验中，动物处死时立即切除对照血管和血管痉挛性血管，并迅速冷冻。随后，使用二维凝胶电泳测量肌球蛋白轻链磷酸化百分比，发现血管痉挛性血管的肌球蛋白轻链磷酸化增加（37%对2%，P < 0.05）。血管痉挛节段中细胞内钙浓度增加和肌球蛋白轻链磷酸化百分比增加表明，平滑肌细胞收缩的钙依赖途径在血管痉挛中起作用。
