dicumarol and Brain-Ischemia

Topics: Brain Ischemia; Cerebrovascular Disorders; Dicumarol; Ethyl Biscoumacetate; Geriatrics; Heparin; Phenindione; Warfarin

A Polycentric International Study was performed to evaluate the diagnostic methods in patients with cerebrovascular diseases. New tools and new non-invasive methods were proposed by the 15 centers collaborating in this study. The difficulty of defining a standard method to investigate not invasively and invasively these patients still remains.

Topics: Brain Ischemia; Brain Neoplasms; Carotid Artery Diseases; Cerebral Angiography; Cerebral Hemorrhage; Cerebrovascular Disorders; Clinical Trials as Topic; Diagnosis, Differential; Dicumarol; Embolism; Heparin; Humans; International Cooperation; Intracranial Aneurysm; Methods; Mitral Valve Prolapse; Plethysmography, Impedance; Ultrasonography

A direct involvement of the antioxidant enzyme NAD(P)H:quinone oxidoreductase (NQO1) in neuroprotection has not yet been shown. The aim of this study was to examine changes, localization and role of NQO1 after different neuronal injury paradigms. In primary cultures of rat cortex the activity of NQO1 was measured after treatment with ethylcholine aziridinium (AF64A; 40 micro m), inducing mainly apoptotic cell death, or oxygen-glucose deprivation (OGD; 120 min), which combines features of apoptotic and necrotic cell death. After treatment with AF64A a significant NQO1 activation started after 24 h. Sixty minutes after OGD a significant early induction of the enzyme was observed, followed by a second increase 24 h later. Enzyme activity was preferentially localized in glial cells in control and injured cultures, however, expression also occurred in injured neuronal cells. Inhibition of the NQO1 activity by dicoumarol, cibacron blue or chrysin (1-100 nM) protected the cells both after exposure to AF64A or OGD as assessed by the decreased release of lactate dehydrogenase. Comparable results were obtained in vivo using a mouse model of focal cerebral ischaemia. Dicoumarol treatment (30 nmol intracerebroventricular) reduced the infarct volume by 29% (p = 0.005) 48 h after the insult. After chemical induction of NQO1 activity by t-butylhydroquinone in vitro neuronal damage was exaggerated. Our data suggest that the activity of NQO1 is a deteriorating rather than a protective factor in neuronal cell death.

Topics: Animals; Apoptosis; Aziridines; Brain Ischemia; Cells, Cultured; Choline; Dicumarol; Disease Models, Animal; Disease Progression; Drug Synergism; Enzyme Activation; Enzyme Inhibitors; Hydroquinones; Male; Mice; Mice, Inbred C57BL; NAD(P)H Dehydrogenase (Quinone); NADPH Dehydrogenase; Neurons; Rats; Rats, Wistar

62 patients with transient ischemic attack (TIA), 60 with reversible ischemic neurologic deficit (RIND) and 57 with stroke with minimum residuum (SMR) were followed, in a retrospective survey, from the first 7 days to the 3rd month of evolution. 90 received anticoagulant treatment, 66 antiplatelet treatment and 23 other or no treatment. 5 patients developed strokes with moderate or severe disability; no patient suffered a myocardial infarction or died. No influence of the type of treatment or of the clinical group (TIA, RIND and SMR) on the follow-up complications could be detected. There seems to be a group with a greater risk of developing further cerebral infarction, which is characterized by the occurrence of multiple TIAs for several days before the event.

Topics: Anticoagulants; Aspirin; Brain Ischemia; Dicumarol; Dipyridamole; Drug Therapy, Combination; Female; Follow-Up Studies; Heparin; Humans; Ischemic Attack, Transient; Male; Middle Aged

Topics: Aspirin; Brain Ischemia; Carotid Arteries; Dicumarol; Dipyridamole; Endarterectomy; Heart Murmurs; Heparin; Humans; Hypertension; Ischemic Attack, Transient; Risk; Sulfinpyrazone; Warfarin