The aim of the study was to verify the production of PAF and the activity of PAF acetyl-
hydrolase (PAF-AH), the
enzyme involved in the catabolism of this
phospholipid mediator, in
migraine attacks. Their levels were determined during
migraine crises in serial samples of internal jugular venous blood taken from five
migraine patients without
aura, who were admitted to the hospital during the crises. Internal jugular venous blood samples were taken immediately after
catheter insertion at 1, 2, and 4 h after attack onset, and within 2 h from its cessation. PAF was purified by high-performance liquid chromatography (HPLC) and determined by radioimmunoassay method. The enzymatic activity of PAF-AH was measured by reverse-phase HPLC, based on the derivatization with 7-diethylaminocoumarin-3-carbonylazide. In the internal jugular venous blood of
migraine patients without
aura (MO), an increase was observed in PAF levels, which was already evident at the time of
catheter insertion (885.6 +/- 82.8) and at the first hour (868.4 +/- 65.24) (ANOVA: P < 0.0001). PAF levels remained elevated through the second (746.8 +/- 82.95), fourth (700.6 +/- 34.93) and sixth hours (644.4 +/- 42.85), and then decreased at the end of the attack, reaching levels significantly lower than those measured at the time of
catheter insertion (565.5 +/- 38.34). The activity of PAF-AH showed an opposite trend with higher values at the first hour and significantly lower values at the second and fourth hours from the beginning of the
migraine attack (ANOVA: P < 0.02). The increased production of PAF may account for persistent platelet activation during
migraine crises, even in the presence of an increased production of
nitric oxide (NO) end-products which, on the other hand, should instead intervene in counteracting and limiting platelet activation. Potential sources of PAF production are the endothelial cells from cerebral vessels, stimulated by trigeminal
neuropeptides, platelets themselves, and mast cells, as suggested by the
neurogenic inflammation model.