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cyclooxygenase/hémorragie
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Aspirin prolongs bleeding time in uremia by a mechanism distinct from platelet cyclooxygenase inhibition.
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We reported that aspirin (ASA) abnormally prolongs bleeding time (BT) in uremia. The present study was designed to investigate whether the abnormally prolonged post-ASA BT in uremia is due to different ASA pharmacokinetics and bioavailability that might be a consequence of uremic condition, platelet
The d-enantiomer form of indobufen totally accounts for the anti-cyclooxygenase and antiplatelet activity ex vivo and for the increase in bleeding time by indobufen in man.
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Indobufen is an antiplatelet drug able to inhibit thromboxane production and cyclooxygenase-dependent platelet aggregation by a reversible inhibition of cyclooxygenase. Indobufen exists in two enantiomeric forms, of which only d-indobufen is active in vitro in inhibiting cyclooxygenase. In order to
Significance of cyclooxygenase-2 elevation in middle cerebral artery for patients with hemorrhagic moyamoya disease.
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The etiology and pathogenesis of moyamoya disease (MMD) remain elusive. Some inflammatory proteins, such as cyclooxygenase (COX)-2, are believed to be implicated in the development of MMD. So far, the relationship between COX-2 and MMD is poorly understood and reports on the intracranial vessels of
Changes in rates of upper gastrointestinal hemorrhage after the introduction of cyclooxygenase-2 inhibitors in British Columbia and Ontario.
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BACKGROUND
Population rates of upper gastrointestinal (GI) hemorrhage have been observed to increase with the introduction and rapid uptake of selective cyclooxygenase-2 (COX-2) inhibitors. Changes in COX-2 inhibitor use and upper GI bleeding rates in regions with relatively restrictive drug
Cyclooxygenase-2 expression on ifosfamide-induced hemorrhagic cystitis in rats.
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OBJECTIVE
Hemorrhagic cystitis (HC) is a limiting side effect of chemotherapy with ifosfamide (IFS). In this study, we investigated the participation of cyclooxygenase-2 (COX-2) upon ifosfamide-induced HC.
METHODS
Male Wistar rats (150-200 g; six rats per group) were treated with saline, IFS (400
Roles of cyclooxygenase-2 in tissue injury during hemorrhagic shock.
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Prostaglandins (PGs), which play a pivotal role in the cytokine network, have been implicated in the pathophysiology of circulatory shock, but the precise role of cyclooxygenase-2 (COX-2) in circulatory shock is still not known. This study investigated whether or not COX-2 affects liver and bowel
Cyclooxygenase-2 expression in the endometrium and its relationship to bleeding in users of continuous oral contraceptives.
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OBJECTIVE
The objective of the present study was to investigate whether or not the presence of irregular bleeding during use of oral contraceptives (OC) is associated with increased cyclooxygenase-2 (COX-2) expression.
METHODS
An observational study was carried out in 26 patients who were using
Assessment of gastric bleeding in rats: effects of cyclooxygenase inhibitors and 16,16-dimethyl prostaglandin E2 on gastric bleeding.
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Gastric bleeding caused by cyclooxygenase inhibitors has been assessed by a novel method. Rats are adapted to a strict light-dark cycle with limited access to food to reduce the stress associated with starvation. Such animals are then labeled with 51Cr-red blood cells from donor animals and dosed
Cyclooxygenase-2 and Prostaglandin E2 are Associated with Middle Cerebral Artery Occlusion and Hemorrhage in Patients with Moyamoya Disease.
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Some inflammatory proteins, such as cyclooxygenase (COX)-2 and prostaglandin (PG) E2 are hypothesized to be implicated in the development of moyamoya disease (MMD). However, the functional roles of COX-2/PGE2 in the pathogenesis of MMD remain elusive. In this study, tiny pieces of middle cerebral
Enhanced cyclooxygenase-2 activity leads to intestinal dysmotility following hemorrhagic shock.
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OBJECTIVE
To test whether hemorrhagic shock (HS) increases the Cyclooxygenase-2 (COX-2) expression in the intestine and whether this enhanced COX-2 expression mediates the intestinal dysmotility after HS.
METHODS
Male Wistar rats were randomly divided into HS sham group and HS group. At 180 min
Cyclooxygenase expression in splanchnic hyposensitivity to glypressin of bleeding portal hypertensive rats.
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BACKGROUND
Prostacyclin mediates, at least partly, the splanchnic vascular hyporesponsiveness to glypressin in bleeding portal hypertensive rats. This study investigated the relative contribution of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in the splanchnic hyposensitivity to glypressin
Inhibition of cyclooxygenase-2 by NS-398 following hemorrhage and subsequent sepsis: no beneficial effects in either gender.
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BACKGROUND
Inhibition of cyclooxygenase-2 with a reduction of prostaglandin E(2)production by the specific antagonist NS-398 has been shown to have beneficial effects on immune function and survival in a trauma model. Immune function after experimental hemorrhagic shock and subsequent sepsis may be
Patent ductus arteriosus, low platelets, cyclooxygenase inhibitors, and intraventricular hemorrhage in very low birth weight preterm infants.
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OBJECTIVE
To assess the risk for intraventricular hemorrhage (IVH) in very low birth weight preterm infants with patent ductus arteriosus (PDA) and low platelet count with treatment with cyclooxygenase (COX) inhibitors.
METHODS
Diagnosis and treatment of PDA, as well as risk factors for IVH, were
Inducible cyclooxygenase expression in canine basilar artery after experimental subarachnoid hemorrhage.
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OBJECTIVE
Inducible cyclooxygenase (COX-2) has been found to play a pathological role in cerebral insult. We investigated the expression of COX-2 in the basilar artery after experimental subarachnoid hemorrhage (SAH).
METHODS
In a canine "two-hemorrhage" model of SAH, the basilar arteries were
Role of Cyclooxygenase-2 in Relation to Nitric Oxide and Endothelin-1 on Pathogenesis of Cerebral Vasospasm After Subarachnoid Hemorrhage in Rabbit.
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Endothelial dysfunctions that include decreased nitric oxide (NO) bioactivity and increased endothelin-1 (ET-1) bioactivity have been considered to be involved in the pathogenesis of cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (SAH). Recent cardiovascular studies have revealed
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