Results 121 to 130 of about 19,044 (171)
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Journal of Neuroscience Nursing, 1980
Because previous studies suggest that prostaglandins (PGs) are involved in the contraction of cerebral arteries, the present study was undertaken to assess the direct effects of arachidonic acid, the precursor of PGs, on isolated dog basilar arteries and to ascertain the actions of three prostaglandin synthesis inhibitors, aspirin, indomethacin, and ...
M K, Gerk, N F, Kassell
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Because previous studies suggest that prostaglandins (PGs) are involved in the contraction of cerebral arteries, the present study was undertaken to assess the direct effects of arachidonic acid, the precursor of PGs, on isolated dog basilar arteries and to ascertain the actions of three prostaglandin synthesis inhibitors, aspirin, indomethacin, and ...
M K, Gerk, N F, Kassell
+6 more sources
Current Opinion in Anaesthesiology, 2016
With recent research trying to explore the pathophysiologic mechanisms behind vasospasm, newer pharmacological and nonpharmacological treatments are being targeted at various pathways involved. This review is aimed at understanding the mechanisms and current and future therapies available to treat vasospasm.Computed tomography perfusion is a useful ...
Ganne S Umamaheswara, Rao +1 more
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With recent research trying to explore the pathophysiologic mechanisms behind vasospasm, newer pharmacological and nonpharmacological treatments are being targeted at various pathways involved. This review is aimed at understanding the mechanisms and current and future therapies available to treat vasospasm.Computed tomography perfusion is a useful ...
Ganne S Umamaheswara, Rao +1 more
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Pathogenesis of Cerebral Vasospasm
Neurological Research, 1980Cerebral arteries have been shown to react to experimental subarachnoid hemorrhage with a nonspecific arterial injury reaction characterized by endothelial cell desquamation, adherence of platelets to the exposed collagen, subendothelial edema, and medial necrosis.
J F, Alksne, P J, Branson
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Neurosurgery Clinics of North America, 1998
Established vasospasm is refractory to vasodilators, although certain agents (nimodipine or papavarine) may reverse early vasospasm when administered in high local concentrations. Calcium channel antagonists do not affect the incidence of arteriographic vasospasm and probably improve outcome by other mechanisms.
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Established vasospasm is refractory to vasodilators, although certain agents (nimodipine or papavarine) may reverse early vasospasm when administered in high local concentrations. Calcium channel antagonists do not affect the incidence of arteriographic vasospasm and probably improve outcome by other mechanisms.
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Contemporary Neurosurgery, 1988
Cerebral vasospasm (specifically, intracranial arterial spasm) is variously defined as: (1) an arteriographically evident narrowing of the lumen of one or more of the major intracranial arteries at the base of the brain due to contraction of the smooth muscle within the arterial wall, or due to the morphological changes in the arterial wall and along ...
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Cerebral vasospasm (specifically, intracranial arterial spasm) is variously defined as: (1) an arteriographically evident narrowing of the lumen of one or more of the major intracranial arteries at the base of the brain due to contraction of the smooth muscle within the arterial wall, or due to the morphological changes in the arterial wall and along ...
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Management of cerebral vasospasm
Neurosurgical Review, 2006Cerebral vasospasm is delayed narrowing of the large arteries of the circle of Willis occurring 4 to 14 days after aneurysmal subarachnoid hemorrhage (SAH). It is but one cause of delayed deterioration after SAH but, in general, is the most important potentially treatable cause of morbidity and mortality after SAH.
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Etiology of Cerebral Vasospasm
1999Cerebral vasospasm is a gradual onset and prolonged constriction of the cerebral arteries in the subarachnoid space after subarachnoid hemorrhage. The principal cause is the surrounding blood clot. The significance of vasospasm is that flow through the constricted arteries may be reduced sufficiently to cause cerebral infarction.
B, Weir, R L, Macdonald, M, Stoodley
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The Pharmacology of Cerebral Vasospasm
Pharmacology, 2008About 3 days after subarachnoid hemorrhage the cerebral blood vessels often undergo a sustained constriction (cerebral vasospasm) which is associated with increased morbidity and mortality. Examination of the literature suggests that interactions of hemoglobin, various prostaglandins, and perhaps some other agents are responsible for this condition ...
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The History of Cerebral Vasospasm
Neurosurgery Clinics of North America, 1990In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain,
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The Nature of Cerebral Vasospasm
Blood Vessels, 2008The article comprises mainly the personal views of the author on the following aspects of cerebral vasospasm: the definition of vasospasm; historical physiological concepts of cerebral bloodflow regulation; relation of spasm development in cerebral arteries to their functional behavior during regulation of cerebral blood flow; the essence of vasospasm ...
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