Essential fatty acid deficiency: A condition to discriminate prostaglandin and non-prostaglandin mediated components of inflammation

Abstract

The carrageenin induced hind paw inflammation is partially suppressed in essential fatty acid deficient (EFAD) rats, but prostaglandin E1 produces larger paw oedema in EFAD rats than in normal ones. Arachidonic acid restores in EFAD rats the suppressed carrageenin inflammation. Shortage of prostaglandin-precursor is the underlying mechanism of reduced carrageenin inflammation in EFAD rats, while the prostaglandin-synthesizing capacity remains unimpaired. BPP9a, a bradykinin potentiating peptide, enhances the carrageenin inflammation in EFAD and control rats equally. The kinin-mediated component of tissue injury is unaltered in EFAD animals, in which the prostaglandin-phase of inflammation is selectively suppressed. Indomethacin does not further reduce in EFAD rats that particular phase of inflammation where prostaglandins are abolished due to precursor shortage. In the preceding period indomethacin exerts partial suppression of inflammation even in EFAD rats. The latter finding supports the view that inhibition of prostaglandin-biosynthesis does not fully explain the antiinflammatory effect of indomethacin.