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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rapid vasicular resistance adjustments in the brain and in the circle of Willis have been continuously measured and enhanced by signal averaging methods. Naftidrofuryl, a drug chemically similar to local anesthetics and to beta adrenergic blocking agents, increases local CBF by reducing resistance in brain and in extracerebral supply arteries. It has also been reported to affect brain metabolism. Other similar drugs merit study for potential effects on CBF and brain metabolism which may be useful in treatment.
Stroke
PMID:Cerebral blood flow regulation. II. Vasodilator mechanisms. 84 83

The effects of naftidrofuryl (LS-121), which is known as an activator of the cerebral glucose metabolism in addition to acting as a cerebral vasodilator on the regional cerebral blood flow (rCBF), were investigated in acute and subacute ischemic stroke patients. Six acute patients and 5 subacute patients were treated with 100-200 mg/day of naftidrofuryl for 7-14 days, and the rCBF was measured before and after the treatment by the 133Xe inhalation method. The hemispheric rCBF was significantly increased by 24% for the acute stage and 22% for the subacute stage in the affected side, compared with the stage-matched control group. Naftidrofuryl may accelerate the recovery of the rCBF of the affected hemisphere even in the acute stage.
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PMID:Effects of naftidrofuryl on the time course of the regional cerebral blood flow in acute ischemic stroke. 654 34

Naftidrofuryl is a selective inhibitor of the 5-HT2 receptor expressed on human endothelial cells. This drug has been used over the years to cope with cerebral or peripheral ischemic accidents; however, no clear mechanism of action of this molecule has been highlighted to explain its vascular effects. In the present work, we demonstrate that the involvement of nitric oxide can account for the effects of naftidrofuryl. Indeed, naftidrofuryl potently inhibited the TNF-alpha-triggered increase of intercellular adhesion molecule-1 (ICAM-1) expression as well as stress fiber formation in human umbilical vein endothelial cells (HUVEC). Moreover, naftidrofuryl induced the expression of type II nitric oxide synthase (NOS II) messenger and protein, leading to a noticeable increase in nitric oxide synthesis. Furthermore, using the specific NOS II inhibitor 1400W, we verified that the observed effects of naftidrofuryl were NOS II-dependent. The biology of nitric oxide accounts for the reduction of the vasospasm associated with stroke and the strong inhibition of platelet aggregation. In conclusion, our work provides evidence for the inhibition of leukocyte recruitment by downregulation of CD54/ICAM-1, an additional key factor to be dealt with during thrombotic accidents. Importantly, it also highlights a novel NOS II-dependent mechanism of action for naftidrofuryl.
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PMID:Naftidrofuryl-driven regulation of endothelial ICAM-1 involves nitric oxide. 1261 50