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The non-adherence of platelets in the circulation has been attributed mainly to two mechanisms : electrostatic repulsion due to net excess negative surface changes on platelets and endothelial cells; and release of endothelial prostaglandin I2 (prostacyclin) which inhibits platelets. CUr experiments were intended to provide evidence on the relative contribution of these mechanisms.  Rabbits were injected with 3H-S-hydroxytryptamine to label the circulating platelets. After about 2h, the rabbits were anaesthetised with nembutal. Both common carotid arteries were constricted in two places about 3 cm apart and perfused free of blood. One common carotid was perfused with saline as control and the other with neuraminidase (from Signa or Behring Werke : 0.5 u/ml saline) for 30 min. These conditions apparently brought about maximal release of sialic acid from the endothelial surface. The constrictions were removed from the arteries to restore the blood flow. After 10 min both carotids were removed. Separate segments were prepared for determinations of radioactivity and prostaglandin I2 and for microscopy.  In seven experiments, the effects of neuraminidase was to increase the deposition of platelets, as measured by their radioactivity, about 4-fold (mean : range 2.0 - 7.3) above controls. Neuraminidase had no significant effect on prostaglandin I2 production, determined by bioassay and radioimmunoassay.  It is concluded that diminution in electrostatic repulsion between circulating platelets and vascular endothelium by removal of sialic acids from, endothelial surface glycoproteins permits adherence of platelets irrespective of prostaglandin I2.

Effect Of Removing Sialic Acid From Vascular Endothelium In Living Animals On Its Interaction With Circulating Platelets