[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
January 16, 1978

Of Platelets, Their Antagonists, and Transient Cerebral Ischemia

Author Affiliations

Scripps Clinic and Research Foundation La Jolla, Calif

JAMA. 1978;239(3):228-229. doi:10.1001/jama.1978.03280300060026

Call me platelet. Consider the lowly platelet if you will— burdened with an undistinguished name, certainly the least interesting of the formed elements of the blood when viewed adjacent to the ebullient eosinophil, the bristling basophil, and the harlequin polymorphonuclear leukocyte. Yet rather than being merely adequate, to cite the laboratory technician's usual cant, it turns out that the platelet is something of a metabolic furnace. It possesses all of the enzymes of the glycolytic pathway, the pentose shunt, and the citric-acid cycle, besides being capable of protein and lipid synthesis.1,2 Platelet functions are equally impressive, including the evolution of clotpromoting activity and the liberation of vasoactive amines that contribute to inflammation.

In a statistical sense, the relationship of transient ischemic attack (TIA) to cerebral infarction is not entirely clear, but to the clinician, it is safe to say that the TIA is a harbinger of a major cerebral