Abstract
The interaction of platelets with damaged vessel walls leads to the formation of platelet-fibrin thrombi and may also contribute to the development of atherosclerotic lesions because platelets adherent to exposed collagen release a mitogen that stimulates smooth muscle cell proliferation. The first step in thrombus formation, platelet adherence to an injured vessel wall, can be studied quantitatively by the use of platelets labeled with 51chromium. In these investigations, rabbit aortas were damaged by passage of a balloon catheter and segments of the aortas were everted on probes that were rotated in platelet suspensions. Collagen-coated glass cylinders were also used. Adherence was measured in a medium containing approximately physiologic concentrations of calcium, magnesium, protein and red blood cells. Conditions of testing influence the effect of non-steroidal anti-inflammatory drugs, sulfinpyrazone, and dipyridamole on platelet adherence. Aspirin and sulfinpyrazone were not inhibitory when tested in a medium with a 40% hematocrit; this indicates that products formed by platelets from arachidonate probably do not play a major part in the adherence of the first layer of platelets to the surface, although they may be involved in thrombus formation.
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Packham, M.A., Cazenave, JP., Kinlough-Rathbone, R.L., Mustard, J.F. (1978). Drug Effects on Platelet Adherence to Collagen and Damaged Vessel Walls. In: Kritchevsky, D., Paoletti, R., Holmes, W.L. (eds) Drugs, Lipid Metabolism, and Atherosclerosis. Advances in Experimental Medicine and Biology, vol 109. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-0967-3_14
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