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Tytuł pozycji:

Platelet activation and lipid peroxidation in patients with acute ischemic stroke

Tytuł :
Platelet activation and lipid peroxidation in patients with acute ischemic stroke
Index Terms :
Acute Disease
Aged
Atrial Fibrillation/blood/metabolism/urine
Brain Ischemia/*blood/*metabolism/urine
Cerebrovascular Disorders/*blood/*metabolism/urine
Cyclooxygenase Inhibitors/therapeutic use
Dinoprost/urine
Female
Humans
Lipid Peroxides/*metabolism
Male
Middle Aged
Platelet Activation
Reference Values
Thromboxane B2/analogs & derivatives/urine
cerebral ischemia
lipid peroxidation
platelet activation
thromboxanes
info:eu-repo/semantics/article
Źródło :
Stroke vol. 28 no. 8, pp. 1557-1563
Wydawca :
1997-08-01
Dodane szczegóły :
Kooten, F. (Fop) van
Ciabattoni, G.
Patrono, C.
Dippel, D.W.J. (Diederik)
Koudstaal, P.J. (Peter)
Typ dokumentu :
Zasób elektroniczny
URL :
http://repub.eur.nl/pub/22518">http://repub.eur.nl/pub/22518
Dostępność :
Open access content. Open access content
info:eu-repo/semantics/openAccess
Pozostałe numery :
QGQ oai:repub.eur.nl:22518
929979401
Źródło wspomagające :
ERASMUS UNIVERSITEIT ROTTERDAM
From OAIster®, provided by the OCLC Cooperative.
Numer akcesji :
edsoai.ocn929979401
Zasób elektroniczny
BACKGROUND AND PURPOSE: Both platelet activation and lipid peroxidation are potential sources of vasoactive eicosanoids that can be produced via the cyclooxygenase pathway, ie, thromboxane (TX) A2, or by free radical-catalyzed peroxidation of arachidonic acid, ie, isoprostanes. We investigated the biosynthesis of TXA2 and F2-isoprostanes, as reflected by the urinary excretion of 11-dehydro-TXB2 and 8-epi-prostaglandin (PG) F2 alpha respectively, in 62 consecutive patients (30 men, 32 women; mean age, 67 +/- 14 years) with acute ischemic stroke. METHODS: At least two consecutive 6-hour urine samples were obtained during the first 72 hours after onset of symptoms. Urinary eicosanoids were measured by previously described radioimmunoassays. RESULTS: Repeated periods of enhanced thromboxane biosynthesis were found in 52% of patients. Urinary 11-dehydro-TXB2 averaged 221 +/- 207 (mean +/- SD; n = 197; range, 13 to 967) pmol/mmol creatinine in 30 patients treated with cyclooxygenase inhibitors (mostly aspirin) at the time of study versus 392 +/- 392 (n = 186; range, 26 to 2533) in 32 untreated patients (P < .001). The corresponding values for 8-epi-PGF2 alpha excretion were 74 +/- 42 (range, 14 to 206) and 83 +/- 65 (range, 24 to 570) pmol/mmol creatinine (P > .05). The correlation between the two metabolites was moderate in both untreated patients (r = .41, P < .001) and patients with cyclooxygenase inhibitors (r = .31, P < .001). In a multiple regression analysis, increased thromboxane production was independently associated with severity of stroke on admission, atrial fibrillation, and treatment with cyclooxygenase-inhibiting drugs. CONCLUSIONS: We conclude that during the first few days after an acute ischemic stroke (1) platelet activation occurs repeatedly in a cyclooxygenase-dependent fashion; (2) platelet activation is not associated with concurrent changes in isoprostane biosynthesis; (3) platelet activation is independently associated with stroke severity and at

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