Inhibition of lipoxygenase (LOX) or of cyclooxygenase (COX) improves survival of rats in endotoxin shock.
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".
Schaper
U
U
Institute of Pathological Biochemistry, Medical Academy Dresden, DDR.
Lueddeckens
G
G
Förster
W
W
Scheuch
D W
DW
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001241:Aspirin / Q000627:therapeutic use*; D016861:Cyclooxygenase Inhibitors; D004195:Disease Models, Animal; D007850:Lauric Acids; D007958:Leukocyte Count / Q000187:drug effects; D008084:Lipoxygenase / Q000627:therapeutic use; D016859:Lipoxygenase Inhibitors; D008297:Male; D010091:Oximes; D010976:Platelet Count / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D012772:Shock, Septic / Q000188:drug therapy* / Q000503:physiopathology; D013929:Thromboxane B2 / Q000097:blood
D016861:Cyclooxygenase Inhibitors; D007850:Lauric Acids; D016859:Lipoxygenase Inhibitors; D010091:Oximes; C059535:FLM 5011; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D008084:Lipoxygenase; D001241:Aspirin