Kinetics of ADP-induced platelet aggregation

Kinetics of ADP-induced platelet aggregation

Vol. 70, Suppl. s59 ABSTRACTS OF 12TH NATIONAL CONGRESS 1 c 109 KINETICS OF ADP-INDUCED PLATELET Landolfi. Centro Fisiopatologia Universita ...

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Vol. 70, Suppl.

s59

ABSTRACTS OF 12TH NATIONAL CONGRESS

1

c 109 KINETICS

OF ADP-INDUCED

PLATELET

Landolfi.

Centro

Fisiopatologia

Universita

Ricerche

Cattolica,

Largo Gemelli

Transmittance evaluation

and

of platelet

formation

impedance

rate

of

occurrence

the

free

platelets

the kinetic

of

this

last

incubated

at

platelets

counts,

after

were

ADP addition,

glutaraldehyde. followed

In all

the

were 7.66i0.85

unchanged. with

This

consistent

platelet

there

under basal

velocities

which allows parameters,

Medica,

for

aggregation. at

conditions

the

free

a standard

error

a very

aggregometer.

platelet

%, respectively.

of the first interesting

the

events tool

0.05

%

concentration

of platelet

while

intervals

with

< 7 %. In 8 normal

of p (85.3+2.4%)

the evaluation

to evaluate

were performed

as at 2 set

suspension

and the percentage and 96.6t3.59

an Elvi

as well

the

, the

by follouing

in order

Experiments

rpm in

vitrot’

conditions

quantitated

the

set

is

1000

conditions

“in

more complex than

approach

of

(v)

per

kinetic “in

far

fixation

was a reduction

method,

aggregation

after

experimental

x103

& R.

Semeiotica

commonly used

by events

We used this

platelet

decay with

platelets

De Cristofaro di

Under the comnon experimental

37’ C and stirred

a single-exponential

pM) ADP concentrations

variations, generated

phenomenon is more directly

performed

at 4 jM ADP, the aggregation (p)

are

of ADP-induced

Electronic

R.

Istituto

00168 Roma, Italy.

in the suspension.

on PRP samples free

8,

bridges.

decay

parameters

dell’Emostasi,

signal

aggregation,

of platelet-platelet

B_ Rocca.

AGGREGATION.

for

subjects,

recruitment At

lower

v values

(1

were

of aggregation investigating

vitro”.

Cl10 DIFFERENTIAL EFFECT OF MODIFIED LDL ON THE EXPRESSION OF PROCOAGULANT ACTIVITY BY MONOCYTES AND ENDOTHELIAL CELLS. p. Madema, E. Stragliotto, S. Colli, M. Camera, F. Bernini and E. Tremoli. E. Grossi Paoletti Center, Institute of Pharmacological Sciences, University of Milan, Italy. Monocyte/macrophages are one of the first cells involved in the pathogenesis of atherosclerosis. Evidence in literature indicates that monocyte/macrophages have a limited number of classical LDL receptors, but express the so called “scavenger” receptors for modified lipoproteins, i.e. acetyl-LDL and oxidized-LDL. In this study, the effects of native and chemically modified LDL on the expression of procoagulant activity (PCA) by human monocytes and human umbilical vein endothelial cells in colture were evaluated. Human monocytes were isolated from the mononuclear cell fraction after adhesion to plastic dishes. Cells were incubated with different concentrations of native and modified LDL (25-200 ug protein/ml) for 6 and 24 hours. The expression of PCA was determined using the one stage clotting assay. Native and oxidized LDL significantly inhibited the expression of PCA by monocytes, the effect being comparable after 6 and 24 hours incubation. On the contrary acetyl-LDL stimulated the basal expression of PCA with a maximal effect obtained using 50 ug protein/ml. Similar effects were observed also when the expression of PCA was evaluated in monocytes coincubated with platelets.The observed effects are cell-dependent since native and acetyl LDL did not inflence the expression of PCA by endothelial cells. At odds to what observed in monocytes, oxidized LDL concentration-dependently stimulated the expression of PCA by endothelial cells. All together these data suggest that native and modified LDL affect PCA expression and that their behaviour is dependent upon the cell considered. In addition, the observation that acet I-LDL are capable to stimulate PCA expreselan by menacytee auggeet a rele far ti le atberegeflle llpegreteins in increasing the potential of this cell to localize fibrin.