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Thromb Haemost 1977; 38(01): 228
DOI: 10.1055/s-0039-1680691
Plenary IV
Thrombosis
Schattauer GmbH

Platelet Prostaglandin Endoperoxides Formation in Hyperlipidemias

R. Bizios
1   Massachusetts Institute of Technology Arteriosclerosis Center, Cambridge, Massachusetts, U.S.A.
2   Cardiac and Hematology Units, Massachusetts General Hospital, Boston, Massachusetts, U.S.A.
,
L.K. Wong
1   Massachusetts Institute of Technology Arteriosclerosis Center, Cambridge, Massachusetts, U.S.A.
2   Cardiac and Hematology Units, Massachusetts General Hospital, Boston, Massachusetts, U.S.A.
,
R. Vaillancourt
1   Massachusetts Institute of Technology Arteriosclerosis Center, Cambridge, Massachusetts, U.S.A.
2   Cardiac and Hematology Units, Massachusetts General Hospital, Boston, Massachusetts, U.S.A.
,
R.S. Lees
1   Massachusetts Institute of Technology Arteriosclerosis Center, Cambridge, Massachusetts, U.S.A.
2   Cardiac and Hematology Units, Massachusetts General Hospital, Boston, Massachusetts, U.S.A.
,
A.C. Carvalho
1   Massachusetts Institute of Technology Arteriosclerosis Center, Cambridge, Massachusetts, U.S.A.
2   Cardiac and Hematology Units, Massachusetts General Hospital, Boston, Massachusetts, U.S.A.
› Author Affiliations
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Publication Date:
16 April 2019 (online)

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    To evaluate the role of prostaglandin endoperoxide formation in the mechanism(s) of platelet hypersensitivity in hyperlipoproteinemias, a study was undertaken in 8 type II patients, 3 type IV, and 8 normal volunteers. Platelet aggregation and release were studied in all subjects. Simultaneously, EDTA-platelets were washed by centrifugation and suspended in modified Ringer’s solution. One ml suspensions (0.8-1x106/μl) were added to 4.5μg of 14C-Arachidonic Acid (AA; sp. act. 50 mCi/mmol) and incubated for 30 sec and 5 min at 37°C. The methylated reaction products were separated by thin layer chromatography. AA, PGE2, PGF2α, and thromboxane B2 (PHD) (Upjohn) were used to identify and locate the respective bands. The products were analyzed by mass spectrometry. TLC-plates were both scanned and scraped for radioactive counting. The chromatograms displayed a pattern similar to that reported by Samuelsson et al. Compared with normal, hypersensitive platelets of type II patients generated 25% more thromboxane A2 (TXA2) after 30 sec incubation with AA, while at 5 min PHD was increased by 30% and TXA2 was still elevated by a factor of 2. The behavior of type IV platelets was similar to normal.

    Aspirin-treated platelets produced one product (HETE). Among the AA derivatives studied, only eluted TXA2 induced platelet release.

    Our data suggest that platelet hyperreactivity in type II patients may be mediated by the increased production and long survival of thromboxane A2.


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