Effects of hyperventilation on prostacyclin formation and on pulmonary vasodilation after group B beta-hemolytic streptococci-induced pulmonary hypertension.

Prostacyclin is released during hyperventilation (HV); however, its role as mediator of HV-induced pulmonary vasodilation remains controversial. We have investigated this by studying the effects of HV on pulmonary artery pressure (PAP) in otherwise normal lungs versus lungs vasoconstricted with group B streptococci (GBS), with and without prior prostacyclin synthesis inhibition. Two- to 3-wk-old piglets were given tranylcypromine, a prostacyclin synthetase inhibitor (n = 6), or placebo (n = 6). Animals were mechanically ventilated normally, then hyperventilated (PCO2 1.5 +/- 0.2 kPa) and then returned to normal ventilation. After each 30-min segment, plasma 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (prostacyclin hydrolysis product) levels and PAP were measured. Then GBS infusions were administered to both groups to induce pulmonary hypertension. With GBS, the normal ventilation/hyperventilation/normal ventilation protocol was repeated as above.(ABSTRACT TRUNCATED AT 250 WORDS)