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[Vincamine in the treatment of minor ictus (due to transient cerebral ischemia)].
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Effect of various classes of drugs on complete ischemia induced by decapitation and cyanide intoxication in mice.
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Effects of various classes of drugs on complete ischemia (gasping) induced by decapitation and cyanide intoxication in mice were investigated. The average gasping duration in complete ischemia and survival time in potassium cyanide injection of control mice were 21.0 +/- 0.1 and 26.1 +/- 0.4 sec
Medical therapy of cerebral ischemia. Vasoactive and eumetabolic therapy.
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After briefly evaluating the contraindications and indications of vasoactive and eumetabolic therapy of cerebral ischemia, the paper considers the main drugs at present in use in therapy of the syndrome induced by diffused cerebral arteriosclerosis. Among the drugs with a mainly vasoactive effect,
[The influence of vincamine on global and regional cerebral blood flow in acute and subchronic human cerebral ischimia (author's transl)].
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The alterations in global and regional cerebral blood flow (CBF) following i.v. application of 14,15-dihydro-14beta-hydroxy-[13alpha,16alpha]-eburnamenine-14-carbonic acid methylester (vincamine) were studied in 18 patients suffering from acute or subchronic cerebral ischemia. CBF measurements were
The effect of ischemia and pharmacological treatment evaluated on synaptosomes and purified mitochondria from rat cerebral cortex.
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Changes in the maximal rate of some cerebral enzymatic activities related to energy transduction (lactate dehydrogenase; citrate synthase and malate dehydrogenase; total NADH-cytochrome c reductase and cytochrome oxidase) as well as both glutamate dehydrogenase and acetylcholine esterase were
Effect of ischaemia and pharmacological treatment on enzyme activities of cortical mitochondria and synaptosomes.
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Changes in the maximal rate of some enzymatic activities related to energy transduction (lactate dehydrogenase; citrate synthetase and malate dehydrogenase; total NADH-cytochrome c reductase and cytochrome oxidase) and others such as glutamate dehydrogenase and acetylcholine esterase were assayed
A comparison of some of the pharmacological properties of the new eburnamenine derivative vindeburnol with those of vincamine, vinburnine, dihydroergotoxine mesilate and nicergoline.
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The effects of a new eburnamenine derivative (3 beta,14 alpha, 16 alpha)-(+/-)-14,15-dihydro-20,21-dinoreburnamenin-14-ol (vindeburnol, RU 24722) on EEG, on brain energy metabolism and on local cerebral blood flow (LCBF) and in different experimental models of cerebral insufficiency were compared
Effects of the new eburnamenine derivative RU 24722 on EEG recovery and cerebral energy metabolism after complete ischemia.
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The influence of a new eburnamenine derivative RU 24722 [(3 beta, 14 alpha, 16 alpha)-(+/-)-14,15-dihydro-20,21-dinoreburnamenin -14-ol] on post-ischemic EEG recovery was studied in N2O anesthetized rats subjected to 1 min of global-compression cerebral ischemia. RU 24722 was compared with
Vinpocetine alleviate cerebral ischemia/reperfusion injury by down-regulating TLR4/MyD88/NF-κB signaling.
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Inflammatory responses play crucial roles in cerebral ischemia/reperfusion injury. Toll-like receptor 4 (TLR4) is an important mediator of the neuroinflammatory response to cerebral ischemia/reperfusion injury. Vinpocetine is a derivative of the alkaloid vincamine and exerts an anti-inflammatory
Brain targeted solid lipid nanoparticles for brain ischemia: preparation and in vitro characterization.
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This study aims at formulating solid lipid nanoparticles (SLNs) of Vinpocetine (VIN) to be used as a brain targeted sustained drug-delivery system. VIN is a derivative of vincamine alkaloid, used for chronic cerebral vascular ischemia. However, it suffers from low bioavailability and short
Influence of hypercapnia on the cerebrovascular activities of some drugs used in the treatment of cerebral ischemia.
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The effects of twelve substances on local cerebral blood flow (LCBF) were studied in the normocapnic and hypercapnic conscious rabbit. In normocapnia, an increase in LCBF was observed after naftidrofuryl (NAF), cinnarizine (CI), viquidil (VI) and heptaminol acefyllinate (HA). The LCBF was only
[Experimental electropharmacologic studies of cerebral ischemia (author's transl)].
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Cerebral aging is associated with psychological and intellectual modifications related to haemodynamic, metabolic disturbances which are often reflected by electroencephalographic alteration (frequency variations, alpha dominant frequency changes). Different tests, based on visual and automatic
Drug interference on some biochemical parameters of rat cerebral cortex during post-ischemic recovery.
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Glycolytic substrates and metabolites (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate), tricarboxylic acid cycle intermediates (citrate, alpha-ketoglutarate, succinate, fumarate, malate), related amino acids (glutamate, glutamine, alanine, gamma-aminobutyrate) and energy mediators (ATP,
[The use of the Mongolian gerbil as a model for cerebrovascular involvement].
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Mongolian Gerbils (Meriones Unguiculatus) are characterized by frequent anomalies of the circle of Willis. Their cerebral vessels lack arterial communication between the cerebral and vertebral system and they present an experimental model for cerebral ischemia. Among drugs which interfere with
Cerebroprotective effect of nicergoline and interference with the anti-hypoxic effect of prostacyclin.
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The cerebroprotective effect of nicergoline was studied using the following experimental methods: hypobaric and anoxic hypoxia in mice, complete ischemia by decapitation in mice, incomplete ischemia by bilateral carotid ligation in rats, hemic hypoxia in rats and asphyxic anoxia in cats. Xanthinol
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