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Thromb Haemost 1995; 74(04): 1175-1179
DOI: 10.1055/s-0038-1649899
Original Article
Vessel Wall
Schattauer GmbH Stuttgart

Oxidized LDL and Reduction of the Antiaggregating Activity of Nitric Oxide Derived from Endothelial Cells

P Minuz
1   The Institutes of Clinica Medica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
C Lechi
2   The Institutes of Chimica e Microscopla Clinica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
S Gaino
2   The Institutes of Chimica e Microscopla Clinica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
S Bonapace
1   The Institutes of Clinica Medica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
L Fontana
1   The Institutes of Clinica Medica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
U Garbin
3   The Institutes of Semeiotica e Nefrologia Medica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
F Paluani
1   The Institutes of Clinica Medica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
L Cominacini
3   The Institutes of Semeiotica e Nefrologia Medica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
M Zatti
2   The Institutes of Chimica e Microscopla Clinica, Policilnico Borgo Roma, University of Verona, Verona, Italy
,
A Lechi
1   The Institutes of Clinica Medica, Policilnico Borgo Roma, University of Verona, Verona, Italy
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Publikationsverlauf

Received 28. März 1995

Accepted after revision 22. Juni 1995

Publikationsdatum:
09. Juli 2018 (online)

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Summary

Oxidized LDL has been observed to induce abnormalities in endothelial function which may be relevant for the progression of atherosclerotic lesions. We studied in vitro the possible effects of oxidized LDL on the antiaggregating activity of endothelial cells, which is dependent on release of prostacyclin and nitric oxide. We used an experimental model in which cultured human endothelial cells were placed in the aggregometer in contact with human platelets, after blockade of cyclo-oxygenase by adding acetylsalicylic acid. In this way the antiaggregant effect of endothelial cells was dependent on the release of nitric oxide alone; prevention of antiaggregant activity by preincubation of endothelial cells with 300 μM L-NG-mono-methyl-arginine confirmed this. When this system was used, endothelial cells (2–7.5 X 105ml) almost completely inhibited thrombin-induced (0.02–0.08 U/ml) platelet aggregation (2 × 108 platelets/ml), measured according to Born (11.1% ±8.5 vs 68.6% ±12.6, M ± SD). This antiaggregating activity was reduced when slightly oxidized LDL 100 μg/ml (35.2% ± 14.9, p <0.001), but not native LDL 100 μg/ml (7.5% ± 7.6), was added immediately before aggregation was induced.. Incubation of endothelial cells with oxidized LDL 100 μg/ml for 1 h did not affect the antiaggregating capacity, unless oxidized LDL was present during aggregation (18.3% ± 10.2 vs 35.8% ± 9.6, p <0.02). No significant direct effect of either oxidized or native LDL on stimulated platelet aggregation was observed. Our results indicate that slightly oxidized LDL can reduce the antiaggregating properties of the endothelium, probably by interaction with NO rather than through inhibition of its synthesis.