American Journal of Physiology-Heart and Circulatory Physiology · 2005 · 45 citations · 52 references
MedicineNeurosciencePharmacologyNeurochemistryNeuropharmacologyPharmacodynamicsCerebral Blood FlowCerebral Vasospasm ManagementCerebrovascular PhysiologyNeurovascular DysfunctionSubarachnoid HemorrhageCerebral Blood Flow AlterationsCerebral Blood Flow EffectsCerebral VasculatureCerebral Vasospasm PhysiologyCerebral Vasospasm PreventionLaser Doppler VelocimetrySubarachnoid Hemorrhage Pharmacotherapy
This study characterized the time course of changes in cerebral blood flow (CBF) and vascular diameter in a dual-hemorrhage model of subarachnoid hemorrhage (SAH) in rats and examined whether acute blockade of the synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE) with N-(3-chloro-4-morpholin-4-yl)phenyl-N'-hydroxyimido formamide (TS-011) can reverse delayed vasospasm in this model. Rats received an intracisternal injection of blood (0.4 ml) on day 0 and a second injection 2 days later. CBF was sequentially measured using laser-Doppler flowmetry, and the diameters of the cerebral arteries were determined after filling the cerebral vasculature with a casting compound. CBF fell to 67% of control after the first intracisternal injection of blood but returned to a value near control 24 h later. CBF again fell to 63% of control after a second intracisternal injection of blood and remained 30% below control for 5 days. The fall in CBF after the second intracisternal injection of blood was associated with a sustained 30% reduction in the diameters of the middle cerebral, posterior communicating, and basilar arteries. Acute blockade of the synthesis of 20-HETE with TS-011 (0.1 mg/kg i.v.), 5 days after the second SAH, increased the diameters of the cerebral arteries, and CBF returned to control. These results indicate that the rats develop delayed vasospasm after induction of the dual-hemorrhage model of SAH and that blockade of the synthesis of 20-HETE fully reverses cerebral vasospasm in this model. They also implicate 20-HETE in the development and maintenance of delayed cerebral vasospasm.
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Initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage.
Joseph Broderick, Thomas G. Brott, John E. Duldner et al. · Stroke · 1994 · 716 citations
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Time course of vasospasm in man
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Production of 20-HETE and Its Role in Autoregulation of Cerebral Blood Flow
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Acute Vasoconstriction after Subarachnoid Hemorrhage
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