Hypoxic vs septic pulmonary hypertension. Selective role of thromboxane mediation

Pulmonary hypertension was generated in 11 newborn piglets, via either infusion of group B beta-hemolytic streptococci (n = 5) or induction of isocapnic hypoxia (n = 6), to study the contributions of thromboxane metabolite thromboxane B2 levels to different types of pulmonary hypertension. After 30 minutes of stable pulmonary hypertension, mean (+/- SD) pulmonary artery pressure increased similarly from 16 +/- 4 to 33 +/- 5 mm Hg (hypoxic), and from 14 +/- 2 to 34 +/- 6 mm Hg (septic). All other measured hemodynamic variables were similar. Despite these hemodynamic similarities, there were significant differences in thromboxane B2 levels. After 60 minutes of pulmonary hypertension, thromboxane B2 levels were 760 +/- 253 pg/mL (hypoxic), and 3103 +/- 1083 pg/mL (septic). These data demonstrate that, while thromboxane appears to be crucial in mediating septic pulmonary hypertension in the piglet, it is not associated with hypoxic pulmonary hypertension, implying that different types of pulmonary hypertension are probably mediated by different biochemical agents.