ChloroquineV1, Main, Exploration, bibRecord, 003343

Pharmacologic modulation of PAF-induced mortality in mice

Identifieur interne : 003343 ( Main/Exploration ); précédent : 003342; suivant : 003344

Pharmacologic modulation of PAF-induced mortality in mice

Auteurs : R. P. Carlson [États-Unis] ; L. O'Neill-Davis [États-Unis] ; J. Chang [États-Unis]

Source :

Agents and Actions [ 0065-4299 ] ; 1987-08-01.

RBID : ISTEX:C57AAFF52790233C7BEFC59181C7EC1740150BFB

English descriptors

Teeft :
- Antagonist, Antioxidant, Antioxidant activity, Dapsone, Diphenyldisulfide, Dose survival, Drug class, Indomethacin, Inhibitor, Inhibitory activity, Isobutylmethylxanthine, Kadsurenone, Lethality, Leukotriene, Mediator antagonists, Mortality model, Ndga, Pharmacologic, Pla2 inhibitor, Platelet, Specific inhibitors, Steroid, Survival rate, Uricosuric agent.

Abstract

Abstract: The effect of antiinflammatory drugs, phosphodiesterase inhibitors, leukotriene and mediator antagonists and other drug classes were evaluated in a PAF-induced mortality model in mice. By the oral route of administration (−1 hr), dapsone (ED50=25 mg/kg), BW 755C (ED50=29 mg/kg), theophylline (ED50=30 mg/kg) and LY-171,883 (ED50=50 mg/kg) protected against PAF-induced lethality in the mouse. Other drugs that afforded protection when given at various dosing schedules and routes were NDGA (100 mg/kg, −18 hr p.o.), diphenyldisulfide (200 mg/kg, −18 hr p.o.), dexamethasone (1 mg/kg, −3 hr p.o.), dipyridamole (2 mg/kg, −2 min i.v.) and kadsurenone (10 mg/kg, −2 min i.v.). Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin were inactive and the combination of AA-861, a putative 5-LO inhibitor, and indomethacin also failed to prevent PAF-induced lethality. Therefore, our pharmacological data do not consistently support the notion that PAF-induced lethality is due unequivocally to leukotrienes derived from 5-lipoxygenase metabolism.

Url:

https://api.istex.fr/ark:/67375/1BB-R47J7Q39-Q/fulltext.pdf

DOI: 10.1007/BF01966521

Affiliations:

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Le document en format XML

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<term>Inhibitory activity</term>
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<front><div type="abstract" xml:lang="en">Abstract: The effect of antiinflammatory drugs, phosphodiesterase inhibitors, leukotriene and mediator antagonists and other drug classes were evaluated in a PAF-induced mortality model in mice. By the oral route of administration (−1 hr), dapsone (ED50=25 mg/kg), BW 755C (ED50=29 mg/kg), theophylline (ED50=30 mg/kg) and LY-171,883 (ED50=50 mg/kg) protected against PAF-induced lethality in the mouse. Other drugs that afforded protection when given at various dosing schedules and routes were NDGA (100 mg/kg, −18 hr p.o.), diphenyldisulfide (200 mg/kg, −18 hr p.o.), dexamethasone (1 mg/kg, −3 hr p.o.), dipyridamole (2 mg/kg, −2 min i.v.) and kadsurenone (10 mg/kg, −2 min i.v.). Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin were inactive and the combination of AA-861, a putative 5-LO inhibitor, and indomethacin also failed to prevent PAF-induced lethality. Therefore, our pharmacological data do not consistently support the notion that PAF-induced lethality is due unequivocally to leukotrienes derived from 5-lipoxygenase metabolism.</div>
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Pharmacologic modulation of PAF-induced mortality in mice

Pharmacologic modulation of PAF-induced mortality in mice

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri