Bevan J A, Bevan R D, Walters C L, Wellman T
Totman Laboratory for Cerebrovascular Research, Department of Pharmacology, University of Vermont, College of Medicine, Burlington, Vermont, USA.
Stroke. 1998 Dec;29(12):2575-9. doi: 10.1161/01.str.29.12.2575.
Animal studies of cerebral arteries 2 to 3 days after experimental subarachnoid hemorrhage (SAH) provide evidence of arterial change such as hyperresponsiveness to contractile agonists. There is evidence that small arteries, as well as those large enough to be seen on angiography, may be involved. To directly test these possibilities, the contractile and dilator responses of pial artery segments taken from patients up to 48 hours after SAH were compared with those from patients having elective surgery for an aneurysm (Clip) and with those from normal brain vessels overlying tumors (controls).
Segments were mounted on a resistance artery myograph for measurements of wall force changes.
There were no differences in maximum contractility (Emax) of the 3 groups of segments. The responses of the SAH segments to K+ (30 mmol/L) were 60.7+/-4.6% of Emax (n [number of vessels]=18), which was significantly greater than those of controls (29.9+/-5% Emax) (n=20). Clip responses were the same as control. Contractions of SAH segments to norepinephrine (1 micromol/L) were 54.3+/-7.9% Emax (n=12), and these were significantly greater than those of controls (15.1+/-6.2% Emax) (n=25). All SAH segments showed spontaneous contractile activity of varying patterns. Spontaneous activity did not occur in the Clip group and occurred in only 50% of control segments. Dilation to acetylcholine was numerically less in SAH and Clip segments than in controls, but differences were not statistically significant. The change in agonist responsiveness could result from exposure to agents that damage the blood vessel wall, resulting in partial depolarization of endothelial and smooth muscle cells.
Small human pial arteries are hyperresponsive to contractile agents and show spontaneous contractile activity within 48 hours of SAH. Such effects could result in narrowed resistance arteries and reduction in cerebral blood flow. These effects emphasize the wisdom of early therapeutic intervention.
对实验性蛛网膜下腔出血（SAH）后2至3天的脑动脉进行的动物研究提供了动脉变化的证据，如对收缩性激动剂的反应性增强。有证据表明，小动脉以及那些大到足以在血管造影中看到的动脉可能都参与其中。为了直接验证这些可能性，将SAH后48小时内患者的软脑膜动脉节段的收缩和舒张反应与因动脉瘤接受择期手术的患者（夹闭组）以及覆盖肿瘤的正常脑血管（对照组）的反应进行了比较。
将节段安装在阻力动脉肌动描记仪上以测量壁力变化。
三组节段的最大收缩力（Emax）无差异。SAH节段对K⁺（30 mmol/L）的反应为Emax的60.7±4.6%（血管数量n = 18），显著大于对照组（29.9±5% Emax）（n = 20）。夹闭组的反应与对照组相同。SAH节段对去甲肾上腺素（1 μmol/L）的收缩反应为Emax的54.3±7.9%（n = 12），显著大于对照组（15.1±6.2% Emax）（n = 25）。所有SAH节段均表现出不同模式的自发收缩活动。夹闭组未出现自发活动，对照组仅50%出现自发活动。SAH和夹闭节段对乙酰胆碱的舒张反应在数值上低于对照组，但差异无统计学意义。激动剂反应性的变化可能是由于接触了损伤血管壁的物质，导致内皮细胞和平滑肌细胞部分去极化。
人软脑膜小动脉在SAH后48小时内对收缩剂反应性增强，并表现出自发收缩活动。这些效应可能导致阻力动脉狭窄和脑血流量减少。这些效应强调了早期治疗干预的明智性。
