Palmitoyl-L-carnitine increases the release of prostacyclin from vascular endothelial cells.

Prostacyclin biosynthesis is dramatically increased in patients with acute myocardial infarction. As palmitoylcarnitine accumulates during myocardial ischemia, the action of this metabolite on the endothelial production of prostacyclin was studied. Palmitoyl-L-carnitine (10-100 microM) enhanced the release of prostacyclin and free arachidonic acid from bovine aortic endothelial cells. This action was mimicked by lysophosphatidylcholine, but by none of the following compounds: acetylcarnitine, carnitine, palmitic acid, sphingosine, dihydrosphingosine and N-stearoyl-dihydrosphingosine. In addition to mobilizing free arachidonate, palmitoylcarnitine induced the release of free choline and phosphorylcholine presumably via the activation of phospholipases C and D. Palmitoyl-L-carnitine had also a cytotoxic effect on the endothelial cells. These data suggest that the increased biosynthesis of prostacyclin in myocardial infarction might be partially explained by the accumulation and release of palmitoyl-L-carnitine.