Diets containing eicosapentaenoic acid and [gamma]-linolenic acids
attenuate cardiopulmonary dysfunction during acute lung injury.
Murray, Michael J., Muthuswamy Kumar, Timothy J. Gregory, Phillip L.
Banks, Henry D. Tazelaar, Stephen J. Demichele.
Department of Anesthesiology and Critical Care Service, Mayo Clinic
and Mayo Foundation, Rochester, MN 55905, and Ross Products Division,
Abbott Laboratories, Columbus, OH 43215
APStracts 2:0291H, 1995.
We examined the effect of substituting linoleic acid (LA) with
eicosapentaenoic acid (EPA) and gammalinolenic acid (GLA), precursors
of trienoic and monoenoic eicosanoids, respectively, on acute lung
injury (ALI). Three groups (n=8/group) of pigs were fed enteral diets
for 8 days containing either LA (Diet A), EPA (Diet B), or a
combination of EPA + GLA (Diet C). ALI was then induced with a 0.1
mg/kg bolus of E. coli endotoxin followed by a continuous infusion
for 4 hours (0.075 mg/kg/hr). Pulmonary arterial and capillary wedge
pressures, cardiac index (CI), arterial blood gases, arterial oxygen
content and plasma thromboxane B2 (TxB2) were measured. PaO2
decreased at 20 min with Diet A. This change was attenuated with
Diets B and C. The EPA and EPA + GLA enriched diets attenuated the
fall in oxygen delivery at 20 minutes, an improvement which was
sustained throughout the 4-hour study period with the EPA + GLA
enriched diet only. This improvement in oxygen delivery was due not
only to the improved PaO2, but also to the maintenance of CI at 20
minutes with Diets B and C and throughout the 4-hour study period
with Diet C. At 4 hours, TxB2 showed a ten-fold increase over
baseline with Diet A, while Diets B and C showed only a three-fold
increase in TxB2. These decreased TxB2 levels with Diets B and C
correlate with an attenuation in the increase in pulmonary vascular
resistance (PVR) that was observed at 20 minutes following endotoxin
infusion with Diet A. These data suggest that specialized enteral
diets enriched in EPA + GLA improve gas exchange and oxygen delivery,
presumably in part through a modification of TxB2 production with a
decrease in PVR and an increase in CI, during ALI.
Received 26 January 1995; accepted in final form 7 June 1995.
APS Manuscript Number H73-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.