Oxygen free radicals are important mediators of both physiological and path
ological events. In acute lung injury, the activated lymphocytes stimulate
tumor necrosis factor (TNF) and other cytokines. These lymphokines augment
free radical generation by polymorphonuclear leukocytes (PMNLs), macrophage
s and other cells which may ultimately produce acute respiratory distress s
yndrome (ARDS). This is supported by our results presented here in that the
re is a significant increase in lipid peroxidation products in patients wit
h established ARDS. The amount of lipid peroxidation was significantly high
er Pn the established ARDS group compared to patients who are at risk for A
RDS. Nitric oxide concentrations were significantly decreased in establishe
d ARDS compared to the control and those who are at risk for ARDS. Fatty ac
id analysis of the plasma phospholipid fraction revealed a significant decr
eased in linoleic acid, gamma-linolenic acid, dihomo-gamma-linolenic acid a
nd arachidonic acid levels of n-6 series and alpha-linolenic acid, eicosape
ntaenoic acid, docosa-hexanenoic acid of n-3 series. Patients who are at ri
sk for ARDS have decreased levels of gamma-linolenic acid of the n-6 series
, alpha-linolenic acid and eicosapentaenoic acid of the n-3 series. These r
esults suggest that lipid peroxides and alteration in essential fatty acid
metabolism may have a role in the pathogenesis of ARDS. (C) 2000 Elsevier S
cience B.V. All rights reserved.