Intralipid alterations in pulmonary prostaglandin metabolism and gas exchange

To assess the role of Intralipid as a prostaglandin (PG) precursor, we infused Intralipid into 40 rabbits with long-term arterial and venous catheters; 24 other rabbits received a control saline infusion. One-half of the rabbits in both experimental and control groups had oleic acid-damaged lungs, and at least 5 in each of the 4 groups (Intralipid/saline in normal/damaged lungs) received indomethacin. Two vasodilating PGs (E₂ and 6KF(1α)) and one vasoconstricting PG (F(2α)) were measured. Triglyceride levels increased significantly in all Intralipid groups, averaging 580 mg/dl. Intralipid-related alterations in PG levels and arterial oxygen tension (PaO₂) were significant only in the lung-damaged group. The mean (± sem) decrease in PaO₂ was 12 ± 1.5 torr (p < .001). For both vasodilating PGs, Intralipid infusion increased the pulmonary arteriovenous gradients for PG E₂ and PG 6KF(1α) by 960 pg/ml (p < .05) and 697 pg/ml (p < .10), respectively. Both the PaO₂ decrease and the vasodilating PG increases were blocked by indomethacin. In summary, Intralipid infusion in lung-damaged rabbits increased pulmonary production of vasodilating PGs and associated hypoxemia, presumably caused by an unblocking of hypoxic vasoconstriction and resultant increase in intrapulmonary right-to-left shunt.