arachidonate/edema

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Suppression by adrenoceptor beta-agonists of vascular permeability increase and edema formation induced by arachidonate metabolites, platelet-activating factor, and tumor-promoting phorbol ester TPA.

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Air-pouch-type inflammation was induced by injecting sodium carboxymethyl cellulose solution containing leukotriene C4 (LTC4, 3.20 x 10(-7) M, 0.2 micrograms/ml) and prostaglandin E2 (PGE2, 5.68 x 10(-6) M, 2.0 micrograms/ml), platelet-activating factor (PAF, 1 x 10(-6) M, 0.52 micrograms/ml), or

Polymorphonuclear leukocyte: arachidonate edema.

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Polymorphonuclear leukocytes (PMN) are important participants in many models of acute lung edema. Enhanced metabolism of arachidonate is also characteristic of many of these models. We found that PMN and arachidonate, but neither alone, increased alveolar capillary permeability of isolated perfused

Involvement of PAF-acether and eicosanoids in adrenaline-induced pulmonary edema in mice.

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The participation of platelet-activating factor (PAF, PAF-acether) in a mouse model of pulmonary edema was studied using specific antagonists. Mice were treated before induction of edema with the PAF antagonists BN52021 (10 mg/kg, ip), PCA4248 (10 mg/kg, po) or WEB2170 (10 mg/kg, ip), the

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

Release of glutamate and of free fatty acids in vasogenic brain edema.

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The pathophysiological potential of mediator substances in manifestations of secondary brain damage is attracting increased attention. This is particularly true of the excitatory transmitters glutamate and arachidonic acid. Noxious properties of these compounds in central nervous tissue have been

Arachidonate metabolic pathways in cells harvested from rat pleural cavity at various times after carrageenan administration.

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Cells were harvested from rat pleural cavity before and during the inflammatory response stimulated by carrageenan injection. The conversion of [14C]arachidonate by intact cells into products of the cyclooxygenase and 5-lipoxygenase pathways was studied in the absence and presence of ionophore.

The pharmacology of arachidonic acid-induced rat paw edema.

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Arachidonic acid (AA) injected into hindpaws of Lewis rats produces a severe edematous response. Treatment with corticosteroids (dexamethasone, prednisolone), dual inhibitors of arachidonate metabolism (phenidone, SK & F 86002), anti-histamine/serotonin agents (chlorpheniramine, cyproheptadine) and

Rat hind-paw swelling effect of an edema-producing protein isolated from Trimeresurus mucrosquamatus snake venom.

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TMV F-IV, isolated from the venom of Trimeresurus mucrosquamatus (TMV), caused rat hind-paw edema in a dose-dependent manner. The maximum hind-paw swelling was reached at 1.5-2 h after subplantar injection of TMV F-IV. The edematous response caused by TMV F-IV was suppressed by the s.c. pretreatment

Pharmaco-modulations of induced edema and vascular permeability changes by Vipera lebetina venom: inflammatory mechanisms.

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The inflammatory response induced by Vipera lebetina venom (VLV) in the mice hind paw was evaluated by paw edema value and vascular permeability changes. The edema was produced in a dose- and time-dependent manner. This response was maximal within 2 h and disappeared after 24 h The minimum

Differential expression of arachidonate 5-lipoxygenase transcripts in human brain tumors: evidence for the expression of a multitranscript family.

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In addition to the important role of leukotrienes as mediators in allergy and inflammation, these compounds are also linked to pathophysiological events in the brain including cerebral ischemia, brain edema, and increased permeability of the blood-brain barrier in brain tumors. Although brain tumors

The effect of the prostaglandin I2 analogue OP-2507 on adrenaline-induced pulmonary edema in rabbits and analysis of hemodynamic changes.

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This study was carried out to understand the onset mechanism of adrenaline (ADR)-induced pulmonary edema (PE) and the effect of drugs related to the arachidonate cascade in a rabbit model. ADR was administered intravenously by a bolus injection to the rabbits at 50, 75 and 100 microg/kg. To evaluate

Eicosapentaenoic acid: effect on brain prostaglandins, cerebral blood flow and edema in ischemic gerbils.

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Eicosapentaenoic acid prevents platelet aggregation and inhibits arachidonate conversion into thromboxane A2 and prostaglandins. Consequently eicosapentaenoic acid might protect the brain from the ischemia that follows cerebral arterial occlusion. We studied the effect of eicosapentaenoic acid on

Dexamethasone effect on free fatty acid and diacylglycerol accumulation during experimentally induced vasogenic brain edema.

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Free fatty acids (FFA), diacylglycerols (DG), and water content were measured in the right and left cerebral hemispheres of rats with brain edema cryogenically induced to the right cerebral hemisphere. The effect of dexamethasone pretreatment was also studied. Twenty-four hours after lesion, maximal

[Peroxidation of arachidonic acid and brain edema].

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Recent studies suggest that peroxidation of arachidonic acid (AA) accumulating during ischemic insult, may be related to the occurrence of post-ischemic brain damage. Since the influence of the increased brain content of AA remains unclear, the present study was undertaken to explore whether the

Vascular permeabilization by intravenous arachidonate in the rat peritoneal cavity: antagonism by ethamsylate.

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The hemostatic agent, ethamsylate, inhibits arachidonic acid metabolism by a mechanism independent of cyclooxygenase activity and blocks carrageenan-induced rat paw edema. Here, ethamsylate was investigated for (i) in vivo actions on the free radical-dependent, permeabilizing responses to

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