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Abstract
Platelets stored for short periods lose in vivo viability. Platelet ATP declines concurrently,
but it is not known whether its decline is due to accelerated degradation, slowed
synthesis, or both. Accordingly, the rate of incorporation of 32Pi into organic compounds (which reflects ATP synthesis) was measured by a modification
of the method of Wadkins and Lehninger. Concurrent measurement of ATP levels allowed
an estimate of its rate of degradation. Platelets suspended in their own plasma maintained
ATP levels for at least 3 hours, during which time the rate of incorporation of 32Pi constantly increased. Thus, ATP levels were maintained at the expense of increasing
synthesis. Washed platelets showed a fall to about 50 per cent of initial values in
3 hours. This was accompanied by a decreasing rate of incorporation of 32Pi. This decrease was not solely due to washing, as washed platelets resuspended in
plasma behaved similarly to platelets maintained in their own plasma. Glucose, added
to washed platelets, stimulated the synthesis of ATP for about one hour, after which
it declined. Palmitate, citrate, and succinate, although rapidly oxidized, did not
stimulate the synthesis of ATP. This was apparently due to uncoupling of oxidation
from phosphorylation. This uncoupling may have resulted from washing and centrifuging
the cells, or could have been due to the anticoagulant used (ACD). It was concluded
that in washed platelets the predominant source of energy is glycolysis, but that
this is probably a consequence of the in vitro uncoupling of oxidative phosphorylation.
In addition, there may be plasma factors that stabilize the metabolism of platelets.
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Article info
Publication history
Accepted:
September 24,
1968
Received:
July 17,
1968
Footnotes
☆Supported in part by United States Public Health Service Grant HE 09057, the American Heart Association, The New Haven and Bridgeport Chapters of The Connecticut Heart Association, and United States Public Health Service Training Grant 5T1GM 696 (Clinical Pathology).
Identification
Copyright
© 1969 Published by Elsevier Inc.
