The increase in vasomotor tone induced by a parenteral lipid emulsion is linked to an inhibition of prostacyclin production.

The aim of the study was to verify whether the infusion of a lipid emulsion causes a rise in vascular pressure related to an imbalance in the production of vasoconstricting and vasodilatating eicosanoids. Segments of umbilical veins were perfused with and without 1.5 microM indomethacin (cyclooxygenase inhibitor) in solutions differing only in their lipid content (control vs. lipid). The lipid-induced higher pressure (p < 0.05) was associated with an inhibition (p < 0.05) in the output of the vasodilatator PGI2, and an increase (p < 0.01) in the production of the vasoconstrictor PGF2 alpha. Indomethacin abolished differences in pressure, but produced a rise (p < 0.01) in vascular tone of both the control and lipid-containing solutions by inhibiting PGI2 synthesis. Prostacyclin was the only eicosanoid significantly correlated (p < 0.01) to vascular tone. The lipid emulsion was therefore linked to the inhibition of the conversion of PGH2 to PGI2. The ensuing greater PGH2 availability would result in vivo, in the increased synthesis of vasoconstricting eicosanoids. The lipid-containing solution produced vasoactive responses similar to those reported with tert-butyl hydroperoxide, suggesting that hydroperoxides contaminating commonly used lipid emulsions could be causing a prostanoid-dependent vasoconstriction.