Hyperventilation, alkalosis, prostaglandins, and pulmonary circulation of the newborn

This study was designed to determine whether the effects of hyperventilation on the pulmonary circulation of the newborn lamb were 1) due to mechanical factors or to respiratory alkalosis; and 2) mediated by prostaglandins. Six control lambs were studied during normal ventilation and during hyperventilation with, and without, decreased carbon dioxide (CO₂). Five lambs were given indomethacin and studied similarly. In control lambs, hyperventilation with decreased CO₂ decreased pulmonary arterial pressure from 26 ± 2.2 to 18 ± 1.0 (SE) Torr (P≤0.005) and pulmonary vascular resistance from 0.099 ± 0.035 to 0.070 ± 0.011 Torr·kg^-1·min^-1 (P≤0.015). Hyperventilation with normal CO₂ did not affect the pulmonary circulation. Hyperventilation with decreased CO₂ increased pulmonary arterial concentrations of 6-ketoprostaglandin F(1α), a major metabolite of prostaglandin, in control lambs but not in the indomethacin-treated lambs. However, it affected the pulmonary circulation of the control- and indomethacin-treated lambs similarly. In conclusion, hyperventilation affected the pulmonary circulation by respiratory alkalosis not by mechanical factors and prostaglandins did not mediate its effects.