The central artery of the rabbit ear was injected with either 1 ml of control or test solutions in a model system which allowed for the study of effluent fractions coming from a segment of the artery and for the examination of the vessel by electron microscopy. The procedure allowed for either mixing of blood with the test solution ("flow by") or injection of the solutions in the absence of blood ("no flow by"). Effluent fractions were collected and assayed for 6-keto-PGF1 alpha, and indicator of PGI2 production. After the collection of effluent fractions, the artery was perfused with 1% glutaraldehyde to begin fixation. Ultrastructural damage to endothelial cells was seen, by SEM, in a graded response to sodium arachidonate solutions at concentrations between 6.6 and 3.3 mM ("flow by"); and between 3.3 and 0.83 mM ("no flow by"). Lower concentrations of arachidonate did not cause damage. Damage included enucleation, separation or denudation of endothelial cells. Sodium linoleate produced similar damage. A burst of PGI2 production appeared to be associated with arachidonate-damaged endothelium. Injection of sodium arachidonate at lower concentrations (0.33 mM and 0.165 mM) resulted in continuous production of PGI2 over a period of 1 to 5 minutes.