Date of Award


Degree Type


Degree Name

Doctor of Philosophy (PhD)


Medical Sciences (Blood and Cardiovascular)


I.A. Feuerstein


R.L. Kinlough-Rathbone


Washed human platelet suspensions were used to study platelet-surface interactions in tubes at wall shear rates between 80 s⁻¹ and 640 s⁻¹ and exposure times up to 900 s. Radiolabeled platelets were used to measure platelet accumulation and release from accumulated platelets as a function of time, shear rate, distance from the inlet of a tube, surface composition and drug treatments of platelets. These empirical data were used in a calculation procedure based upon diffusion and convection, designed to yield the maximum interfacial fluid concentration (IFC) for each of the materials which are liberated from platelets during platelet accumulation upon surfaces. Substances such as AMP, ATP, serotonin, pyrophosphate, PGG₂ and PGH₂ were found not to be present in sufficient quantity to produce IFC's which could affect platelet aggregation. A second set of materials, von Willebrand factor, fibronectin, and calcium had IFC's less than the concentrations normally found in plasma. A third group, ADP, PGD₂, and TA₂ had IFC's close to those known to affect platelet aggregation. These last materials, along with materials formed by a vessel wall or in plasma are most likely to determine the rate of thrombus growth on subendothelium or on a blood-contacting biomaterial.

As well, epi-fluorescent video microscopy was used to monitor platelet-surface interactions with different surfaces giving different spectrums of results.

[table removed]

Aspirin, sulfinpyrazone, indomethacin and PGE₁ treatment of platelets inhibited aggregate formation on a collagen surface but not platelet adhesion. Heparin, hirudin, imipramine, mepacrine, adenosine triphosphate, creatine phosphate/creatine phosphokinase treatment of platelets had no or little effect on adhesion, release or aggregate formation. Modification of platelet functions using pharmacological and suspension modification techniques demonstrated mural aggregate formation was independent of release of adenosine diphosphate by adherent platelets but dependent on prostaglandin and thromboxane formation.

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