Balloon catheter technique for dilatation of constricted cerebral arteries after aneurysmal SAH
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Cerebral Vasospasm
Cerebral circulation
Cerebral Vasospasm
Cisterna magna
Animal model
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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
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Cerebral vasospasm is a common serious complication after subarachnoid hemorrhage, and is one of the main reasons of morbidity and mortality in patients suffering from subarachnoid hemorrhage. However, However, its pathogenesis has not yet been fully elucidated. Recent studies have suggested that apoptosis plays an important role in the mechanism of cerebral vasospasm. Further study of the apoptotic mechanism of cerebral vasospasm following suharachnoid hemorrhage has important significance for the optimization of therapeutic schemes in clinical conditions.
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cerebral vasospasm; subarachnoid hemorrhage; apoptosis
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The delayed cerebral vasoconstriction known as cerebral vasospasm remains a significant cause of permanent neurological deficit and death following aneurysmal subarachnoid hemorrhage despite the best current medical therapies. The mechanism of cerebral vasospasm remains unknown. Several new drugs have been tested in animal models of subarachnoid hemorrhage, and these experimental studies have contributed to a better understanding of the potential mechanisms that lead to cerebral vasospasm. In this article, the authors highlight recent advances in the various treatment procedures for delayed cerebral vasospasm following subarachnoid hemorrhage. (c) 2001 Prous Science. All rights reserved.
Cerebral Vasospasm
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Cerebral vasospasm is the most common and most dangerous complication of subarachnoid hemorrhage (SAH). If it can not be diagnosed and treated early, it will result in delayed cerebral ischemia and delayed ischemic neurological deficits, and seriously affect the outcomes of patients. SAH can cause oxidative stress and inflammation, causing vasospasm, and leading to brain tissue damage. Numerous studies have shown that the concentrations and activities of numerous metabolites will change in these pathological physiological processes. Identification of the changes of location, time and trend of these markers has important clinical significance for investigating the mechanism of cerebral vasospasm after SAH and seeking better therapeutic targets. This article reviews the molecular markers of cerebral vasospasm after SAH.
Key words:
Subarachnoid Hemorrhage; Vasospasm, Intracranial; Biological Markers
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Objective To investigate the pathogenesis treatment and prognosis of cerebral vasospasm due to subarachnoid hemorrhage. Method In this research ,we studied cerebral vasospasm group(n=42)and controlled group(n=50)without cerebral vasospasm due to subarachnoid hemorrhage, used Nimodipine to treat CVS,meanwhile, observed the curative effect and estimated the prognosis. Results There is no marked difference in age and sex between two groups(P0.05). Most patient with CVS were occurred within 2 weeks. There was 34 cases of 42 cases whose cerebral ischemic symptom was disappeared and 8 cases were death. The mortality of CVS group is higher than controlled group(P0.05). Conclusion Cerebral vasospasm due to subarachnoid hemorrhage could mostly be reversed by early detection, exactly diagnosis and treatment.
Nimodipine
Cerebral Vasospasm
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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
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