Vol. 276, Issue 3, R659-R664, March 1999
Effect of prostanoids and their precursors on the aggregation
of rainbow trout thrombocytes
D. J.
Hill1,
M. B.
Hallett2, and
A. F.
Rowley1
1 School of Biological
Sciences, University of Wales Swansea, Singleton Park, Swansea SA2 8PP;
and 2 Department of Surgery,
University of Wales College of Medicine, Heath Park, Cardiff CF4
4XN, United Kingdom
The role of
prostanoids and their precursor fatty acids in the aggregatory response
of thrombocytes (platelet equivalents of fish) from the rainbow trout,
Oncorhynchus mykiss, was studied. Aggregation of these cells was induced by the thromboxane mimetic U-46619 or arachidonic acid (AA) in the presence of human or trout fibrinogen. The production of
TXB2/3 by thrombocytes in response to stimulation with AA was inhibited by aspirin, ibuprofen, and indomethacin. However, thrombocyte aggregation in response to AA
stimulation was not significantly altered by these agents at the
concentrations tested (10-100 µM), with the exception of
indomethacin at 20 and 40 µM. Effects on cytosolic calcium
concentration have been suggested as an alternative mechanism for the
inhibitory action of indomethacin on human platelet aggregation. The
present study, however, failed to identify this as a mechanism for the inhibition of U-46619-induced trout thrombocyte aggregation by indomethacin. The polyunsaturated fatty acids docosahexaenoic acid and
eicosapentaenoic acid both exhibited an inhibitory effect on
U-46619-induced thrombocyte aggregation similar to that observed with
mammalian platelets. Unlike the case in mammalian hemostasis, prostacyclin inhibited thrombocyte aggregation only at high
concentrations (>5 µM). Prostaglandin
E2, however, inhibited thrombocyte
aggregation at much lower concentrations (>0.01 µM), suggesting
that it may be the major inhibitory eicosanoid in trout.
eicosanoids; platelet equivalent; hemostasis; fish
