Thromb Haemost 1994; 71(05): 627-632
DOI: 10.1055/s-0038-1642494
Review Article
Schattauer GmbH Stuttgart

Serum Lipid Profile Determines Platelet Reactivity to Native and Modified LDL-Cholesterol in Humans

Per L Katzman
1   The Department of Medicine, Section of Nephrology, Winnipeg, Canada
,
Ratna Bose
2   The Department of Pharmacology and Therapeutics, Winnipeg, Canada
,
Stephen Henry
1   The Department of Medicine, Section of Nephrology, Winnipeg, Canada
,
Donna L McLean
3   The Department of Medicine, Lipid Clinic, Winnipeg, Canada
,
Shaun Walker
1   The Department of Medicine, Section of Nephrology, Winnipeg, Canada
,
Christopher Fyfe
2   The Department of Pharmacology and Therapeutics, Winnipeg, Canada
,
Yvette Perry
1   The Department of Medicine, Section of Nephrology, Winnipeg, Canada
,
David Mymin
3   The Department of Medicine, Lipid Clinic, Winnipeg, Canada
,
Peter Bolli
1   The Department of Medicine, Section of Nephrology, Winnipeg, Canada
› Author Affiliations
Further Information

Publication History

Received 29 October 1991

Accepted after revision 31 January 1994

Publication Date:
06 July 2018 (online)

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Summary

The effects of thrombin (0.2 U/ml) and native (n-LDL), malon- dialdehyde-modified (MDA-LDL) and auto-oxidized (ox-LDL) low-density lipoproteins (20 μg of protein/ml) on platelet activation were evaluated in seven hyperlipidemic patients and compared to seven controls (fasting serum cholesterol 8.49 ± 0.5 and 4.61 ± 0.4 mM, respectively). Basal and thrombin-induced increases in platelet intracellular free calcium ion concentration ([Ca2+; fura-2) were similar in hyperlipidemic patients and controls (45 ± 5 vs 42 ± 3 and 635 ±51 vs 599 ± 69 mM, respectively). n-LDL, MDA-LDL and ox-LDL increased basal [Ca2+]; (16, 36 and 81 percent, p <0.01 between LDL-types), increases were consistently smaller in patients. There was an inverse relationship between LDL-induced responses and fasting serum LDL cholesterol as well as LDL/HDL ratio.

In conclusion, modified LDL activated platelets to a greater extent than n-LDL, suggesting different types of LDL-receptors. Their agonistic effect was inversely related to the fasting serum lipid profile, suggesting that blunting of platelet responses to LDL could represent a protective mechanism in hyperlipidemic patients.