thesis
Studies on human blood platelets
- Publication date
- Publisher
Abstract
This
project was undertaken to increase the understanding of platelet function, with
paticular emphasis on abnormal platelets in diabetes mellitus, and improving the quality of
platelet concentrates for transfusion.
{1} Potential
platelet antagonists,
including PGE1,
verapamil,
insulin
and
hirudin,
were added to platelet concentrates
in
an attempt to
improve
the recovery and shelf-life of the
concentrate.
Each "preservative"
caused some
improvement in
platelet concentrate quality, as
measured
by functional
tests, and radio-immunoassay
for the platelet activation marker,
B-
thromboglobulin. The best
results were obtained with the addition of
PGE1,
which
facilitated
recovery of all samples to which
it
was added, suggesting a cheap way of ensuring
consistently good platelet concentrates.
{2} Various investigations
were carried out regarding abnormal platelet
function in
diabetes mellitus.
No
significant
differences
were
found in
the responses of platelets
from
diabetics
and age-matched controls to the calcium-channel
blocking drug, Verapamil, in
vitro.
Similarly, the
capacity of
diabetic
platelets to produce malondialdehyde, a
by-product
of thromboxane
A2
synthesis, was not significantly
different from
control platelets.
The
use of insulin
in
aggregometry studies showed, surprisingly, that
insulin
could
have
a pro-aggregatory effect on platelets
from diabetics, but
not
those
from healthy
controls.
In
addition, evidence
for the existence of a platelet aggregation-enhancing
factor in
the
plasma of
diabetics
and older controls was obtained.
{3} Extensive
tests to
investigate
the nature of spontaneous platelet aggregation
(SPA) in
whole
blood have
established the existence of two types of
SPA, (i) ADP-dependent, and
(ii)
ADP-independent. The
results obtained suggest a major role
for
erythrocytes in the
development
of
inappropriate
platelet aggregation
