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    Constrictive structural elements in human cerebral arteries following aneurysmal subarachnoid haemorrhage
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    Abstract:
    Histoimmunological, histochemical, and histological studies were conducted on cerebral arteries from four living patients with a recent aneurysmal subarachnoid haemorrhage. There appeared to be a correlation between the severity of vasospasm and the magnitude of pathological findings. Large myofibroblast cells and type V collagen within the medial layer were abundant in arteries showing marked vasospasm, but were less conspicuous in those showing milder involvement. Intracranial arteries from patients who died from non-cerebral causes did not demonstrate these changes. In ruptured vessels, there was also a positive fluorescence for actin-myosin filaments in layers of the arterial wall other than the media. It is postulated that the intimal and adventitial actin-myosin, myofibroblasts and type V collagen may contribute to cerebral vasospasm by holding the damaged vessel in a contracted phase during the healing period.
    Keywords:
    Myofibroblast
    Cerebral Vasospasm
    Anterior cerebral artery
    Delayed release of hemoglobin from the subarachnoid clot in the vicinity of conductive arteries leads to cerebral vasospasm after SAH. The mechanism of vasospasm however remains unclear. The one thousand times higher affinity of ferrous heme for nitric oxide, a potent vasodilator of cerebral vessels, than to oxygen, has led to the concept that hemoglobin scavenges nitric oxide and produces delayed cerebral vasospasm after SAH. For several years we have investigated the pathological mechanism(s) behind this event using in vivo experiments. We summarize experimental data and discuss the clinical value of the observations for the development of a new treatment for vasospasm after SAH.
    Cerebral Vasospasm
    The performance of transcranial Doppler in the detection of anterior cerebral artery vasospasm and vasospasm in patients after subarachnoid haemorrhage was analysed. Transcranial Doppler and cerebral angiography were performed within the same 24 hours on each of 41 patients with acute subarachnoid haemorrhage. Sensitivity and specificity of transcranial Doppler to classify middle cerebral arteries, anterior cerebral arteries, and patients with angiographic vasospasm were determined at mean velocities of 120 and 140 cm/s. Accuracy of transcranial Doppler was better at 140 than at 120 cm/s. For the middle cerebral artery, sensitivity was 86%, specificity 98%. For the anterior cerebral artery, sensitivity was 13%, specificity 100%. Among all patients, sensitivity was 45%, specificity 96%. Among patients with anterior communicating artery aneurysms, sensitivity was 14%, specificity 90%. Therefore, transcranial Doppler accurately differentiates between middle cerebral arteries with and without vasospasm on angiography, but has a very low sensitivity for detecting anterior cerebral artery vasospasm and vasospasm in patients with anterior communicating artery aneurysms. Since vasospasm may involve anterior cerebral arteries while sparing middle cerebral arteries, especially after rupture of an anterior communicating artery aneurysm, caution should be exercised in using negative transcranial Doppler results to make treatment decisions based on the assumed absence of vasospasm.
    Transcranial Doppler
    Anterior cerebral artery
    Anterior communicating artery
    Cerebral Vasospasm
    Citations (68)
    BACKGROUND: Cerebral vasospasm is delayed-onset cerebral arterial narrowing in response to blood clots left in the subarachnoid space after spontaneous aneurysmal subarachnoid hemorrhage (SAH). Ideally, studies on the pathogenesis and treatment of cerebral vasospasm in humans should be conducted using human cerebral arteries. Because in vivo experiments using human vessels are not possible, and postmortem pathological examination of human arteries in vasospasm provides only a limited amount of information, a number of animal models of vasospasm have been developed. METHODS: The literature was searched to find all references to in vivo animal models of SAH and vasospasm. An online search of the medical database MEDLINE was initially performed using the key words "cerebral," "vasospasm," "subarachnoid," "hemorrhage," "animal," and "model." References were checked to determine the first description of each in vivo animal model. RESULTS: Fifty-seven models of SAH and vasospasm were identified. These models used one of three techniques to simulate SAH: 1) an artery was punctured allowing blood to escape and collect around the artery and its neighbors; 2) an artery was surgically exposed, and autologous blood obtained from another site was placed around the artery; or 3) blood from another site was injected into the subarachnoid space and was allowed to collect around arteries. Each technique has advantages and disadvantages. The majority of animal models of SAH and vasospasm use intracranial arteries; however, extracranial arteries have also been used recently in vasospasm experiments. These studies seem easier and less costly to perform, but concerns exist regarding the physiological dissimilarity between systemic and cerebral arteries. CONCLUSION: The model of SAH and vasospasm used most frequently is the canine "two-hemorrhage" model, in which two injections of blood into the dog's basal cistern performed 48 hours apart result in greater arterial vasoconstriction than that effected by a single injection of blood. On the basis of its ability to accurately predict what occurs in human SAH, the best model of vasospasm seems to be the primate model in which a blood clot is surgically placed around the large cerebral vessels at the base of the monkey's brain.
    Cerebral Vasospasm
    Subarachnoid space
    Objective: A multitude of subarachnoid hemorrhage (SAH) models have been described but only several of them are still in use. All models to a different degree helped in understanding of pathophysiology of cerebral vasospasm after SAH. Their advantages and drawbacks have been reviewed in this paper. Since 2000, when the last review on cerebral vasospasm in animal models was written, new animal models of SAH were introduced and our knowledge about pathophysiology of CVS improved. The aim of present review was to update the information about well established and newly implemented models of vasospasm after SAH. Materials and methods: The MEDLINE searches were carried out using keywords that included 'subarachnoid hemorrhage', 'animal', 'model', as well as names of animal species such as 'rats', 'dogs', 'mice', 'rabbits', 'pigs' or animal groups, e.g. 'non-human primates'. Owing to a limited volume, only models of SAH in vivo were included in our review. Results: We identified 53 original models of SAH in considered groups of animals. For the past several years, use of rats and mice became increasingly common in vasospasm studies due to advancements of imaging techniques, new approaches in vessel morphometry and reduced costs related to small animals. However, dog model of SAH is still considered superior for vasospasm studies as the ability of murine models to model human vasospasm is disputed. Conclusion: Testing new concepts of vasospasm etiology will require re-evaluation of in vivo models of CVS. The updated knowledge about their advantages and limitations is necessary for effective design in future studies of cerebral vasospasm after SAH.
    Cerebral Vasospasm
    Animal model
    Pathophysiology
    Etiology
    Human studies
    Animal studies
    Citations (77)
    ✓ The effect of phenoxybenzamine (PBZ) on cerebral vasospasm of the basilar artery induced by the injection of 2 ml of blood into the cisterna magna of dogs was assessed in chronic experiments. The presence of vasospasm was documented arteriographically. In one group of animals, 12 mg/kg of PBZ was given intravenously 2 hours before the intracisternal injection of blood to ascertain whether this drug would prevent the development of vasospasm for 24 hours. In another group of animals a 10 −2M solution of PBZ was given intracisternally 15 minutes after vasospasm was produced, and again 24 hours afterward, to determine if the drug would reverse an existing spasm. These drug-treated animals were compared with controls which were treated with saline alone. The results indicate that the drug treatment was not statistically superior to saline in any of the groups studied. The finding that saline injected into the cisterna magna reversed the cerebral vasospasm illustrates the importance of this procedure in evaluating effectiveness of drugs and confirms the original observation that washing the cerebrospinal fluid with saline can terminate an experimentally induced vasospasm. Moreover, the fact that intracisternal injections of saline were more effective when given soon after the establishment of vasospasm than when injected 24 hours afterward supports the conclusion of others that the pathogenesis of cerebral vasospasm changes with time. The results also indicate that the presence of cerebral vasospasm in some animals did not prevent the return of normal behavior.
    Cisterna magna
    Cerebral Vasospasm
    Phenoxybenzamine
    Citations (23)
    The removal of subarachnoid clot has been thought to be effective for prevention of cerebral vasospasm. However, it is suggested that the incidence of cerebral vasospasm is not high in the cases where ruptured cerebral aneurysms are obliterated using Guglielmi detachable coils (GDC) without clot removal. The effect of subarachnoid clot removal on the occurrence of cerebral vasospasm and the different incidence of cerebral vasospasm between clipping cases and in GDC cases are reviewed.Surgical clot removal in experimental model indicated marked preventive effect on cerebral vasospasm. However, the clinical trials of clot removal during early aneurysm surgery had failed to show satisfactory preventive effect for vasospasm, and the cumulative incidence of symptomatic vasospasm in these trials was 29%. As fibrinolytic drug, intrathecal administration of tissue plasminogen activator showed sufficient elimination of subarachnoid clot and prevention of cerebral vasospasm in the experimental studies and in the clinical case trials and nonrandomized case-control trials. However, the multi-center, randomized case-control trial showed no statistically significant effect on symptomatic cerebral vasospasm. On the other hand, the cumulative incidence of cerebral vasospasm in GDC cases was 20%. The comparative studies of the incidence of vasospasm between GDC cases and in clipping cases also showed less incidence of symptomatic vasospasm and a more favorable outcome in GDC cases. From the results of studies reviewed, the incidence of cerebral vasospasm seems less in GDC cases than in clipping cases. It should be clarified why clipping could not be dominant in the prevention of cerebral vasospasm compared to GDC.
    Cerebral Vasospasm
    Clipping (morphology)
    Citations (5)
    Objective To investigate the relationship between the development ofA1 segment of the anterior cerebral artery and the communicating artery. Methods A total of 107 subjects underwent 3.0 T magnetic resonance angiography(MRA) were involved in this study. The development of the anterior cerebral artery and the state of communicating artery were observed. The diameter of A1 segment of the anterior cerebral artery and the communicating artery, Correlation between them were analyzed. Results 1Hypoplastic left and right anterior A1 segments of the cerebral artery were respectively 16.82%(18/107)and22.43%(24/107). Absence of the left and right anterior cerebral arteries were 1.87%(2/107)and 0.93%(1/107). 2 51 patients with the anterior communicating artery was developed. 3 39 patients with single or bilateral posterior communicating arteries were developed, among them 21 cases developed bilaterally, 7cases developed on the left and 11 cases on the right. 4 The development of the communicating artery was correlated with the development of A1 segment of anterior cerebral artery(r=0.654,P0.01). Conclusions The hypoplasia of A1 segment of the anterior cerebral artery leads to compensatory development of the communicating artery.
    Anterior cerebral artery
    Anterior communicating artery
    Magnetic resonance angiography
    Posterior cerebral artery
    Posterior communicating artery
    Citations (0)