Systemic and portal prostacyclin and thromboxane response to hemorrhage in portal hypertension.

Prostacyclin (PGI2) and thromboxane (Tx-A2) levels increase in hemorrhagic shock. Prostanoids have been implicated as mediators of the systemic and splanchnic hyperemia characteristic of portal hypertension (PHT). We hypothesized that prostanoid pharmacokinetics could be altered during shock in PHT and mediate the poor tolerance of PHT animals to hemorrhage. Hemodynamics and PGI2 and Tx-A2 levels were determined in portal, systemic venous, and arterial vascular beds at baseline and following hemorrhage and resuscitation. Portal and systemic PGI2 levels were elevated at baseline in PHT animals, with no change in resting Tx-A2. Following hemorrhage, PGI2 and Tx-A2 levels increased in normal animals, but were unchanged in PHT. Portal hypertension PGI2 production was elevated at rest, while Tx-A2 levels were diminished. There is a diminished prostanoid response to hemorrhage in PHT animals compared to normal. This abnormality in prostanoid pharmacokinetics may contribute to the abnormal response to hemorrhage in PHT.