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PLATELET MEMBRANE MUCOPOLYSACCHARIDES: SOME RELEVANT OBSERVATIONS *
Author(s) -
O'Brien John R.
Publication year - 1972
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1972.tb16308.x
Subject(s) - platelet , ruthenium red , chemistry , neuraminidase , membrane , glycosaminoglycan , biochemistry , glycoprotein , aspirin , biophysics , sialic acid , staining , platelet rich plasma , calcium , biology , immunology , enzyme , medicine , pathology , organic chemistry
Summary Biochemical analysis disorganizes the membrane before study; thus there are advantages in studying reactions of intact cells. Alcian blue (AB) causes aggregation of washed red cells–presumably because of membrane staining and a charge effect. Neuraminidase or the presence of plasma prevents this aggregation. AB added to platelets without plasma causes immediate aggregation; added to platelet‐rich plasma at low concentration, it potentiates ADP‐induced aggregation. A higher concentration stains the granules and causes release and delayed aggregation. Aspirin inhibits release induced by ADP but hardly influences that induced by AB. This suggests that aspirin inhibits an early stage of release, since adding AB shows that the later stages are still intact. During release, platelet factor 4, a glycoprotein, is liberated. Thereafter the platelet membrane stains with ruthenium red, but not before. Neuraminidase removes sialic acid. It prevents red cells but not platelets from aggregating with AB, and it exposes platelet factor 3 sites on platelets but not on red cells. These findings are believed to relate to the organization of mucopolysaccharides and glycoproteins in the platelet membrane.