© 1996 American Heart Association, Inc.
Articles |
Lipoprotein(a) Inhibits Collagen-Induced Aggregation of Thrombocytes
From the Institutes of Physiology (A.G., M.G., H.W., T.K.) and Medical Biochemistry (G.M.K.), Graz, Austria, and the Department of Hematology (M.I., J.J.S.), University Hospital Utrecht, Utrecht, Netherlands.
Correspondence to Dr Anna Gries, Institute of Physiology, Harrachgasse 21/V, 8010 Graz, Austria.
Abstract Lipoprotein(a) [Lp(a)] is known to interact with
human platelets in vitro. In the present study the effect of
physiological concentrations of Lp(a) on
platelet aggregation was studied. Freshly prepared gel-filtered
platelets from healthy donors were incubated for 30 minutes at
37°C with various concentrations of Lp(a); aggregation was triggered
with ADP, thrombin, and collagen. Control incubations were performed
with Tyrode's solution or LDL. Thrombin- and ADP-triggered
aggregations were only slightly influenced by Lp(a), but aggregation of
platelets stimulated with collagen (4 µg/mL) was markedly
inhibited. Measurable effects occurred at low concentrations (0.05
mg/mL) of total Lp(a); at 0.5 mg/mL, maximum aggregation of
platelets was inhibited by 54±20%, and the aggregation rate was
attenuated by 47±19% compared with platelets incubated with
Tyrode's solution. Preincubation of collagen (4 µg/mL) with Lp(a)
yielded similar results. The effect of Lp(a) on platelet
aggregation was accompanied by a significant reduction of
serotonin release and TXA2 formation. Higher
concentrations of collagen (
10 µg/mL) caused the
inhibitory effect of Lp(a) on collagen-induced
aggregation to disappear. In contrast, incubation of platelets with
5 mg/mL LDL led to a significant increase of aggregation rate, maximum
aggregation, serotonin release, and formation of
TXA2 when aggregation was induced with 4 µg/mL collagen.
In an adhesion assay using fresh whole blood, which mimics the in vivo
situation of vessel injury, Lp(a) reduced platelet adhesion at
shear rates of 300 and 1600/s by 22.6% and 11.6%, respectively. In
addition, Lp(a) reduced the size of platelet aggregates
significantly (up to 63%); this reduction was more distinct at the
higher shear rate. Unlike LDL, Lp(a) is not a proaggregatory
lipoprotein; rather, collagen-triggered aggregation in vitro is
attenuated by Lp(a).
Key Words: lipoprotein(a) • platelet aggregation • serotonin release • thromboxane A2 • platelet adhesion
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