1. Evidence suggests that activation of phospholipase A2 and production of eicosanoids and platelet-activating factor (PAF) are involved in various responses associated with severe tissue damage and shock. It was postulated that the plasma level of the precursor and degradation product of PAF, lyso-platelet-activating factor (lyso-PAF), might be increased in acute severe illness.
2. After plasma extraction, lyso-PAF was acetylated in vitro to PAF, which was measured by bioassay using 5-[14C]hydroxytryptamine-labelled rabbit platelets. Measurements were made in 18 severely ill patients (five with cardiogenic shock; five with severe infection, five after repair of abdominal aortic aneurysm, two with acute pancreatitis; 13 males, five females). Plasma lyso-PAF in these patients was 33 ± 15 (sd) ng/ml (range 5–111 ng/ml), whereas values in normal males (40–65 years) ranged from 102 to 253 ng/ml (n = 15) and in females from 74 to 174 ng/ml (n = 10). Depression of plasma lyso-PAF did not relate closely to the patient group nor to specific therapy, but repeated measurements in each of 10 patients showed an increase in plasma lyso-PAF (P < 0.002), associated with clinical improvement.
3. Evidence was obtained indicating that neither the presence of an inhibitor in the assay system nor reconversion of PAF to lyso-PAF in vitro produced the unexpected depression of plasma lyso-PAF.
4. The mechanisms responsible, which may have therapeutic implications, remain to be elucidated.