Agents and Actions

, Volume 21, Issue 3–4, pp 379–381 | Cite as

Pharmacologic modulation of PAF-induced mortality in mice

  • R. P. Carlson
  • L. O'Neill-Davis
  • J. Chang
Mediators of Acute Inflammation

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.

Keywords

Dexamethasone Indomethacin Theophylline Antiinflammatory Drug Dipyridamole 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. [1]
    J. M. Young, P. J. Maloney, S. N. Jubb and J. S. Clark,Pharmacologic investigation of the mechanisms of platelet activating factor induced mortality in the mouse. Prostaglandins30, 545–551 (1985).CrossRefPubMedGoogle Scholar
  2. [2]
    T. Yoshimoto, C. Yokoyama, K. Ochi, S. Yamamoto, Y. Maki, Y. Ashida, S. Terao and M. Shiraishi,2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA861) A selective inhibitor of the 5-lipoxygenase reaction and the biosynthesis of slow-reacting substance of anaphylaxis. Biochim. Biophys. Acta713, 430–473 (1982).Google Scholar
  3. [3]
    S. M. Coutts, A. Khandwala, R. Van Inwegen, U. Chakraborty, J. Musser, J. Bruens, N. Jariwala, V. Dally-Meade, R. Ingram, T. Pruss, H. Jones, E. Neiss and I. Weinryb,Arylmethylphenyl ethers — A new class of specific inhibitors of 5-lipoxygenase. InProstaglandins, leukotrienes and lipoxins (Ed. J. M. Bailey). Plenum Press, New York 1985.Google Scholar
  4. [4]
    D. Kelefiotis and C. Vakirtzi-Lemonias,Effect of non-steroidal antiinflammatory drugs on alkyl-acetyl-glycerol-phosphorylcholine-induced anaphylactic shock in mice. Biochem. Soc. Transactions14, 94–95 (1986).Google Scholar
  5. [5]
    Y. Ashida, T. Saijo, H. Kuriki, H. Makino, S. Terao and Y. Maki,Pharmacological profile of AA-861, a 5-lipoxygenase inhibitor. Prostglandins26, 955–972 (1983).CrossRefGoogle Scholar
  6. [6]
    R. J. Gordon, J. Travis, H. R. Godfrey, D. Sweeney, P. S. Wolf, T. P. Pruss, E. Neiss, J. Musser, U. Chakraborty, H. Jones and M. Leibowitz,In vivo activity of a lipoxygenase inhibitor and leukotriene antagonist, REV 5901-A. Leukotrienes Prostaglandins84, 266 (1984).Google Scholar
  7. [7]
    J. C. Foreman,The pharmacological control of immediate hypersensitivity. Ann. Rev. Pharmacol. Toxicol.21, 63–81 (1981).CrossRefGoogle Scholar

Copyright information

© Birkhäuser Verlag 1987

Authors and Affiliations

  • R. P. Carlson
    • 1
  • L. O'Neill-Davis
    • 1
  • J. Chang
    • 1
  1. 1.Immunopharmacology Subdivision, Division of Experimental TherapeuticsWyeth Laboratories, Inc.PhiladelphiaUSA

Personalised recommendations