Dizdarević Kemal
Department of Neurosurgery, University of Sarajevo Clinics Centre, Sarajevo, Bosnia and Herzegovina.
Bosn J Basic Med Sci. 2008 May;8(2):177-82. doi: 10.17305/bjbms.2008.2978.
Intracranial aneurysmal rupture is the common cause of spontaneous subarachnoid haemorrhage (SAH). This haemorrhage is typically diffuse and located in extracerebral subarachnoid space in which main cerebral arterial branches are situated. The intimate and long-term contact of arterial wall and blood products in the closed space causes the cerebral vasospasm as a serious and frequent complication of SAH. It is connected with significant morbidity and mortality due to developing of focal cerebral ischaemia and subsequently cerebral infarction. The aim of our experimental research was to create the animal model of vasospasm using the femoral artery due to examination of reduced basic dilator activity cause in arterial wall after SAH. The important characteristic of major cerebral arteries is their localization in the closed subarachnoid space which enables their to have long-term contact with blood products after haemorrhage. Thirty six femoral arteries (FA) of eighteen female rats weighing about 300 g were used. In vivo, femoral arteries are microsurgically prepared in both inguinal regions in all rats. Eighteen arteries were encompassed by polytetrafluoroethylene (PTFE) material forming closed tube and autologous blood was injected in the tube around the arterial wall. Additional eighteen arteries, as a control group, were also put in PTFE tube but without exposing to the blood. All rats are left to live for eight days. Afterwards, rats were sacrificed and their arteries were in vitro examined including an isometric tension measurement and histological changes analysis. The tension was measured during application of vasoconstrictors and vasodilatators (nitric oxide, NO). FA exposed to periadventitial blood exhibit hyper reactivity to constrictors (KCl, phenylephrine, acetylcholine) compared to control group. It was also found that NO donor (sodium nitroprusside) diminished arterial spasm induced by blood and vasoconstrictors. In conclusion, FA can be used as a model for vasospasm correlating with cerebral vasospasm after SAH and therefore this model can be utilized in future experiments assessing cerebral vasospasm. The reduced basic dilator activity of spastic femoral artery is caused by an absence of gaseous messenger NO next to the arteries but not by diminished response vasculature to NO. Absence of NO after SAH probably causes the reduced basic dilator activity of cerebral arteries as well. The guanylate-cyclase level in the arterial wall is consequently reduced after SAH primary due to absence of NO but not due to direct reduction of enzyme activities caused by process of blood degradation inside of subarachnoid space.
颅内动脉瘤破裂是自发性蛛网膜下腔出血（SAH）的常见原因。这种出血通常是弥漫性的，位于脑外蛛网膜下腔，主要脑动脉分支也位于此。在这个封闭空间内，动脉壁与血液成分的密切和长期接触会导致脑血管痉挛，这是SAH一种严重且常见的并发症。它与因局灶性脑缺血进而发展为脑梗死导致的显著发病率和死亡率相关。我们实验研究的目的是通过使用股动脉创建血管痉挛的动物模型，以研究SAH后动脉壁基础舒张活性降低的原因。大脑主要动脉的一个重要特征是它们位于封闭的蛛网膜下腔内，这使得它们在出血后能够与血液成分长期接触。使用了18只体重约300克的雌性大鼠的36条股动脉（FA）。在所有大鼠体内，通过显微手术在双侧腹股沟区域制备股动脉。18条动脉被聚四氟乙烯（PTFE）材料包裹形成封闭管，并在管壁周围的管内注入自体血。另外18条动脉作为对照组，也置于PTFE管中，但不接触血液。所有大鼠存活8天。之后，处死大鼠并对其动脉进行体外检查，包括等长张力测量和组织学变化分析。在应用血管收缩剂和血管舒张剂（一氧化氮，NO）期间测量张力。与对照组相比，暴露于外膜周围血液的股动脉对收缩剂（氯化钾、去氧肾上腺素、乙酰胆碱）表现出高反应性。还发现NO供体（硝普钠）可减轻血液和血管收缩剂诱导的动脉痉挛。总之，股动脉可作为与SAH后脑血管痉挛相关的血管痉挛模型，因此该模型可用于未来评估脑血管痉挛的实验。痉挛性股动脉基础舒张活性降低是由于动脉旁气态信使NO的缺失，而非血管系统对NO的反应减弱。SAH后NO的缺失可能也会导致脑动脉基础舒张活性降低。SAH后动脉壁中鸟苷酸环化酶水平最初降低主要是由于NO的缺失，而非蛛网膜下腔内血液降解过程直接导致酶活性降低。
