cyclooxygenase/edema

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Cyclooxygenase-2 inhibitors: a new therapeutic option in the treatment of macular edema after cataract surgery.

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Two patients had uneventful phacoemulsification. After initial improvement, vision deteriorated because of cystoid macular edema (CME). In 1 patient, treatment with systemic nonsteroidal antiinflammatory drugs showed significant improvement in visual acuity but had to be discontinued because of side

Synergistic effect of nitric oxide synthase and cyclooxygenase inhibitors on carrageenan-induced paw edema in rats.

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The present study examined the effects of L-nitroarginine methylester (L-NAME, CAS 50903-99-6), a non-selective nitric oxide synthase (NOS) inhibitor, indometacin (IND, CAS 3305-29-1), a non-selective cyclooxygenase (COX) inhibitor, and a combination of these agents (L-NAME + IND) on

Effect of antirheumatics and inhibitors of cyclooxygenase, lipoxygenases and thromboxane synthetase on cobra venom factor rat paw edema.

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The cobra venom factor (CVF) rat paw edema was inhibited by cyclooxygenase (indomethacin, piroxicam, aspirin), lipoxygenase (BW 755c) and thromboxane synthetase (imidazole) inhibitors as well as by dexamethasone and, at high doses, by paracetamol and phenacetin. No definite results were obtained

Cyclooxygenase inhibition in lungs or in neutrophils attenuates neutrophil-dependent edema in rat lungs perfused with phorbol myristate acetate.

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Results from previous studies indicate that injury in isolated rat lungs perfused with buffer containing phorbol myristate acetate (PMA) and rat neutrophils (PMNs) is dependent on the production of reactive oxygen species and thromboxane (Tx) A2. The purpose of this study was to determine whether

Inhibition of cyclooxygenase 2 by nimesulide decreases prostaglandin E2 formation but does not alter brain edema or clinical recovery after closed head injury in rats.

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Recently, the enzyme cyclooxygenase (COX) has been recognized to exist as constitutive (COX-1) and inducible isoforms (COX-2). In previous studies, drugs that were inhibitors of both COX-1 and COX-2 failed to decrease brain edema formation or improve Neurological Severity Score (NSS) after closed

Cyclooxygenase metabolites contribute to oleic acid-induced lung edema by a pressure effect.

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We investigated the role that lung-derived arachidonic acid metabolites play in the acute changes in pulmonary hemodynamics, airway function, and lung fluid balance following oleic acid-induced injury in the isolated blood free perfused lung. A bolus injection of oleic acid (OA) emulsion (12 mg)

[Simultaneous and sequential inhibition of the arachidonic acid cascade by inhibitors of phospholipase A2, cyclooxygenase and lipoxygenases in carrageenan edema and adjuvant arthritis in the rat].

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According to the aim of the simultaneous and sequential inhibition of key enzymes of the arachidonic acid cascade, combinations of inhibitors of the phospholipase A2 (PLA2), cyclooxygenase (COX) and of lipoxygenases (LOX) were administered to rats with carrageenin edema and adjuvant arthritis,

Edema from cyclooxygenase products of endogenous arachidonic acid in isolated lung.

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We infused A23187, a calcium ionophore, into the pulmonary circulation of dextran-salt-perfused isolated rabbit lungs to release endogenous arachidonic acid. This led to elevations in pulmonary arterial pressure and to pulmonary edema as measured by extravascular wet-to-dry weight ratios. The

Vitex negundo inhibits cyclooxygenase-2 inflammatory cytokine-mediated inflammation on carrageenan-induced rat hind paw edema.

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BACKGROUND Vitex negundo L. (Verbenaceae) is a hardy plant widely distributed in the Indian subcontinent and used for treatment of a wide spectrum of health disorders in traditional and folk medicine, some of which have been experimentally validated. In present study, we aimed to investigate the

Lung edema due to hydrogen peroxide is independent of cyclooxygenase products.

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Active oxygen species can cause lung injury. Although a direct action on endothelial cells is proposed, the possibility exists that they might cause injury via mediators. We considered that active oxygen species would stimulate the generation of cyclooxygenase metabolites, which then alter pulmonary

Synthesis and amelioration of inflammatory paw edema by novel benzophenone appended oxadiazole derivatives by exhibiting cyclooxygenase-2 antagonist activity.

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Ten new 2(4-hydroxy-3-benzoyl) benzamide-5-phenyl-1,3,4-oxadiazole derivatives (10a-j) were synthesized by coupling 3-benzoyl-4-hydroxybenzoic acid (5) with 2-amino-5-phenyl-1,3,4-oxadiazoles (9a-j). The structures of these compounds were confirmed by IR, 1H, 13C NMR, and mass spectra, and also by

Physician-reported management of edema and destabilized blood pressure in cyclooxygenase-2-specific inhibitor users with osteoarthritis and treated hypertension.

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BACKGROUND The addition of a nonsteroidal anti-inflammatory drug to the regimen of a patient with treated hypertension can cause a destabilization of blood pressure. OBJECTIVE The aim of this study was to describe physician-reported management of clinically significant edema and/or destabilized

Electroacupuncture inhibits inflammatory edema and hyperalgesia through regulation of cyclooxygenase synthesis in both peripheral and central nociceptive sites.

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We investigated the anti-inflammatory effects of electroacupuncture (EA) on carrageenan-induced inflammatory model in association with peripheral and spinal COX-2 expression. EA with 2, 15 and 120 Hz, especially 2 Hz, had significant inhibitory effects on the developing of edema and hyperalgesia,

Radiation-induced edema is dependent on cyclooxygenase 2 activity in mouse brain.

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Cerebrovascular dysfunction, characterized by compromise of the blood-brain barrier and formation of cerebral edema, is common during the acute period after brain irradiation and may contribute to delayed pathology (e.g. vascular collapse, white matter necrosis) that leads to functional deficits.

Modulation of mouse ear edema by cyclooxygenase and lipoxygenase inhibitors and other pharmacologic agents.

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Inhibitors of arachidonic acid (AA) metabolism and other pharmacologic agents were evaluated against ear edema produced in mice by tetradecanoylphorbol acetate (TPA) or AA. Drugs were administered orally and topically either 30 min prior to AA or 30 min after TPA, except for steroids which were

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