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Human or rabbit platelets were activated by ADP or 5-hydroxytrypatamine and rapidly fixed with glutaraldehyde. The shape change associated with activation gave rise to an increase in sialic acids removable by neuraminidase. This increase, like the shape change, was prevented by adenosine or methysergide added before ADP or 5-hydroxytryptamine respectively. The results indicate the exposure of additional glycoprotein(s) on the platelet surface.

Radiolabelled oligosaccharides prepared as described by Hall & Patrick ( 19 88) were separated on a Biogel P2 ( < 400 mesh) column, 60 cm x 0.9 cm, eluted with water and 0.5 ml fractions collected. The initial sample ( I ) and aliquots of fractions were separated on silica gel t.1.c. plates run in butanol/acetic acid/water (2: 1 : 1, by vol.). The void volume was at fraction 30, with glucose eluting at fraction 66.

The enzymically catalysed incorporation of N-acetylneuraminic acid into human platelets, whether suspended in their own citrated plasma or in buffered saline containing 0.17 mM-sucrose, accelerated the uptake of 5-hydroxytryptamine. This acceleration decreased with time. The observations may be explained by assuming that N-acetylneuraminic acid is a component of a transport receptor for 5-hydroxytryptamine.

followed by trouser tear tests using specimens partially cut along their longitudinal axis. Force is applied to the free ends in opposite directions, gradually tearing the tissue apart. Information on tissue viscoelasticity is provided by equilibrium force extension measurements. This is achieved by extending the tissue over set time intervals with intermittent periods when the distance between the clamps is held constant. While the clamps are held static, tissue relaxation is observed. Our study on human atherosclerotic plaque caps involved stress-strain analyses on test strips ( 10 mm x 2 mm) punched with their long axis in the circumferential direction from intact central and peripheral plaque areas, and adjacent intima. The cap or intima was carefully dissected away from the underlying elastic lamina before mounting for mechanical testing. The results show marked differences between plaques and heterogeneity within individual plaque caps. Fracture stresses in different plaques ranged from 12 to 1938 kN m-*. Intra-plaque stress and strain values indicated discontinuity in the mechanical properties across the plaque cap in both ulcerated and non-ulcerated plaques. The magnitude of these differences was more pronounced in the ulcerated group. Biochemical analysis of mechanically tested areas within the eight non-ulcerated plaques highlighted a trend for collagen content to coincide with increased fracture stress and reduced extensibility. A similar sized group of ulcerated plaque caps failed to show these trends. Sulphated glycosaminoglycan content did not correlate with mechanical parameters in non-ulcerated plaques, but its decrease in the centres of ulcerated plaques accompanied a reduction in fracture stress and increase in extensibility. The mechanical testing device used in conjunction with biochemical analysis is a valuable tool in pinpointing the determinants of atherosclerotic plaque cap rupture.