Summary
The bleeding diathesis and abnormalities of platelet aggregation in the Fawn-Hooded
(FH) rat, as in human patients with storage pool disease, have been attributed to
decreased amounts of adenine nucleotides that are ordinarily stored with serotonin
in the platelet dense granules. This study was undertaken in order to establish whether
the platelet defect of the FH rat was present in young platelets, newly emerged from
the bone marrow, or whether the platelets acquired this abnormality (possibly by a
premature release reaction) during their circulation in the blood. FH and Wistar rats
were made thrombocytopenic with one injection of anti-platelet serum (APS) and platelets
were harvested during the recovery phase. The ATP content of “young” FH platelets
harvested two days after injection of APS, was higher than that of platelets obtained
from untreated FH rats, but was still only 50% of that found in “young” Wistar platelets.
In addition, the adenine nucleotide content of FH platelets did not change during
treatment with aspirin. “Young” FH platelets were also deficient in serotonin and,
unlike Wistar platelets, their serotonin content did not increase appreciably with
the increasing platelet age. The results of the study strongly suggest that the defect
in FH platelets is present in platelets newly emerged from the bone marrow and is
not due to premature release of the “storage” contents during their circulation in
the blood.
