CHEMISTRY AND FUNCTIONS OF PROSTACYCLINS AND

THROMBOXANES
Prostacyclins Vs. Thromboxanes: Both prostacyclins (PG-I2) and
thromboxanes (Tx) are produced from cyclic endoperoxide PG-H2 (Fig. 5.5 and
5.6). Cyclic endoper- oxide first formed in PG synthesis is PG-G2, which is
converted to PG-H2, an immediate precursor of PGI2 and Tx. Both cyclic
endoperoxides have a very short 1⁄2 life (t1⁄2 = 5 minutes at 37°C) but they are
biologically very active, and have powerful effect on contraction of GI smooth
muscles, bronchial muscles and umbilical cord vessels. Main differentiating
points between prostacyclins (PGI2) and thromboxane (Tx) are shown in Table
5.1.

Applied Aspect of PG-I2 and Tx

1. Prevention of thrombus formation in health: Platelets attempting to stick to blood

vessel wall release endo- peroxides, which is converted to prostacyclin (PG-I2) by
endothelial cells of blood vessel wall. PH-I2 by its vaso- dilatation effects and
inhibition of platelet aggregation, repel the platelets and prevent them from
sticking and forming a “nidus” and thus opposes thromboxane activity. A
balance between these two biochemical processes is critical for the thrombus
formation.

2. Injury to blood vessel wall: Injury to blood vessel wall decreases PG-I2 formation
and thus reduces the anti- aggregatory action of PG-I2. Unopposed action of TX-
A2 in such cases cause platelet aggregation and thrombus formation.