Inhibition of lipoxygenase (LOX) or of cyclooxygenase (COX) improves survival of rats in endotoxin shock.

Abstract

In a well defined endotoxin (ET) shock model we compared the influence of a selective LOX-inhibitor FLM 5011 and the COX-inhibitor Acetylsalicylic acid (ASA) on survival as well as on their effects on TXB2 and 6-oxo-PGF1 and on selected parameters characterizing the shock syndrome. Pretreatment with both substances reduced the lethality rate. Neither TXB2 nor the PGF1 concentration revealed a consistent trend after therapeutic intervention. None of the investigated mediators could be identified as the primary "shock mediator".

• Authors: U Schaper, G Lueddeckens, W Förster, D W Scheuch
• Journal: Biomedica biochimica acta (Biomed Biochim Acta) Vol. 47 Issue 10-11 Pg. S282-5 ( 1988) ISSN: 0232-766X [Print] Germany
• PMID: 3150270 (Publication Type: Journal Article)

Chemical References

• Cyclooxygenase Inhibitors
• Lauric Acids
• Lipoxygenase Inhibitors
• Oximes
• FLM 5011
• Thromboxane B2
• 6-Ketoprostaglandin F1 alpha
• Lipoxygenase
• Aspirin

Topics

• 6-Ketoprostaglandin F1 alpha (blood)
• Animals
• Aspirin (therapeutic use)
• Cyclooxygenase Inhibitors
• Disease Models, Animal
• Lauric Acids
• Leukocyte Count (drug effects)
• Lipoxygenase (therapeutic use)
• Lipoxygenase Inhibitors
• Male
• Oximes
• Platelet Count (drug effects)
• Rats
• Rats, Inbred Strains
• Shock, Septic (drug therapy, physiopathology)
• Thromboxane B2 (blood)