Effect of removing sialic acids from endothelium on the adherence of circulating platelets in arteries in vivo

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Abstract
The contribution of the net negative charge excess due to sialic acids on endothelium in preventing adhesion of circulating platelets in vivo was investigated in anesthetized rabbits. Platelets in the rabbit''s circulation were selectively labeled with radioactive 5-hydroxytryptamine in vivo. Segments of carotid arteries temporarily isolated from the circulation were perfused with 1 of 2 commercial preparations of neuraminidase; the opposite carotid artery was perfused similarly without the enzyme, as control. A neuraminidase preparation from Behringwerke free of proteolytic activity released sialic acid into the perfusate with a peak concentration after 10-15 min which decreased gradually later. A neuraminidase preparation from Sigma that contained demonstrable proteolytic activity released sialic acid similarly during the 1st hour and thereafter more sialic acid in a second peak. After blood flow through the carotids had been restored, the adhesion of labeled platelets in the artery perfused with neuraminidase was compared with that in the artery perfused without the enzyme. The radioactivities were significantly higher in carotids perfused with neuraminidase than in those perfused without the enzyme. Neuraminidase perfusion had no effect on the production of prostacyclin by the carotids. Perfusion with acetylsalicylic acid before neuraminidase increased the adhesion of platelets significantly. Diminution in electrostatic repulsion between circulating platelets and vascular endothelium from which the net negative charge excess due to sialic acids has been removed increases the adhesion of circulating platelets, irrespective of the production of prostacyclin by the arterial walls, and inhibition of prostacyclin production augments this platelet adhesion.