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Innovations in aneurysmal subarachnoid hemorrhage: intracisternal t-PA for the prevention of vasospasm.

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Aneurysmal subarachnoid hemorrhage (SAH) affects approximately 30,000 people each year in North America. At least 30% of these patients will develop vasospasm as a result of the initial hemorrhage, and two thirds of these develop permanent disabilities or die. Blood deposited into the basal cisterns

An overview of new pharmacological treatments for cerebrovascular dysfunction after experimental subarachnoid hemorrhage.

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Cerebral vasospasm and the resulting cerebral ischemia occurring after subarachnoid hemorrhage (SAH) are still responsible for the considerable morbidity and mortality in patients affected by cerebral aneurysms. Mechanisms contributing to the development of vasospasm, abnormal reactivity of cerebral

Vasospasmogenic substance produced following subarachnoid haemorrhage, and its fate.

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Fresh blood and supernatants of blood-CSF mixtures incubated for 1 to 15 days were applied to the basilar artery of adult cats, and the degree of constriction was measured with a surgical microscope. The constriction due to fresh blood was weak and transient. It seems possible to assume that

Effect of experimental subarachnoid hemorrhage on CSF eicosanoids in the rat.

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A simple and inexpensive experimental model of subarachnoid hemorrhage (SAH) was developed in the rat. Based on accumulating data indicating the important role of arachidonic acid metabolites in the etiology of delayed cerebral vasospasm, we investigated changes induced by SAH on cerebrospinal fluid

Effects of common medications on cerebral vasospasm after subarachnoid haemorrhage.

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Cerebral vasospasm is a common and serious complication of aneurysmal subarachnoid haemorrhage (SAH). At present, no consistently effective preventative and therapeutic measures are available, perhaps because of incomplete understanding of the pathogenesis of vasospasm. Experimental studies provide

Red blood cells are essential for late vasospasm following experimentally induced subarachnoid hemorrhage in dogs.

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The in vivo spasmogenic activity of various blood components was examined in dogs. Each blood fraction was injected into the cisterna magna at 0.5 or 1.0 ml/kg body weight, after the removal of 0.5 ml/kg body weight of cerebrospinal fluid, and vertebral angiography was then performed. Whole blood

Expression of vascular endothelial growth factor (VEGF) in rat brain after subarachnoid haemorrhage and endothelin receptor blockage with BQ-123.

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Cerebral vasospasm is one of the most severe complications of subarachnoid haemorrhage (SAH), leading to pathological changes in the vessel wall itself and in the nervous tissue, due to ischaemia of endothelial cells and neurones. Amongst the known substances inducing vasospasm, the most potent

Erythropoietin for the treatment of subarachnoid hemorrhage: A feasible ingredient for a successful medical recipe.

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Subarachnoid hemorrhage (SAH) following aneurysm bleeding accounts for 6% to 8% of all cerebrovascular accidents. Although an aneurysm can be effectively managed by surgery or endovascular therapy, delayed cerebral ischemia is diagnosed in a high percentage of patients resulting in significant

Effect of recombinant streptokinase on the development of chronic cerebral vasospasm after subarachnoid hemorrhage in a swine model.

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BACKGROUND After subarachnoid hemorrhage (SAH), the formation of subarachnoid clots and their associated resolution may be involved in the development of chronic cerebral vasospasm. To dissolve and wash out the subarachnoid clot is one of the therapeutic strategies for prevention of cerebral

Endothelin and subarachnoid hemorrhage: an overview.

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BACKGROUND Delayed cerebral vasospasm occurring after subarachnoid hemorrhage (SAH) is still responsible for a considerable percentage of the morbidity and mortality in patients with aneurysms. It has been suggested that the pathogenesis of delayed cerebral vasospasm is related to a number of

Role of ferrous iron chelator 2,2'-dipyridyl in preventing delayed vasospasm in a primate model of subarachnoid hemorrhage.

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OBJECTIVE Oxyhemoglobin (HbO2) causes vasospasm after subarachnoid hemorrhage (SAH). The most likely spasmogenic component of HbO2 is iron. Various iron chelators, such as deferoxamine, have prevented vasospasm in vivo with limited success. However, only chelators of iron in the ferric state have

Cisternal irrigation therapy with urokinase and ascorbic acid for prevention of vasospasm after aneurysmal subarachnoid hemorrhage. Outcome in 217 patients.

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BACKGROUND Cisternal irrigation therapy with urokinase and ascorbic acid was introduced to prevent symptomatic vasospasm after aneurysmal subarachnoid hemorrhage (SAH). To dissolve and wash out the subarachnoid clot, cisternal irrigation with urokinase is used. Ascorbic acid is added to degenerate

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

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Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be

Platelet-derived growth factor-induced severe and chronic vasoconstriction of cerebral arteries: proposed growth factor explanation of cerebral vasospasm.

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OBJECTIVE After subarachnoid hemorrhage (SAH), platelet-derived growth factor-BB (PDGF-BB) is secreted in and around the cerebral arteries. To clarify the role of PDGF-BB in the development of vasospasm after SAH, we determined whether PDGF-BB alone can cause long-lasting vasoconstriction of a

The three phases of vasospasm.

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We propose the theory that prolonged cerebral vasospasm involves three phases: (1) the initial muscular contraction of the arterial wall; (2) a secondary injury to the artery that consists of endothelial desquamation with adherence of platelets to te denuded internal elastic lamina and mural

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