Vasodilators or vasoconstrictors prevent hypoxic pulmonary vasoconstriction

Abstract

Prostaglandins modulate pulmonary vascular resistance (PVR) and hypoxic pulmonary vasoconstriction (HPV). We studied the effects of a prostaglandin vasodilator (PGI 2) and vasoconstrictor (PGE 2) in the pulmonary circulation and compared these effects to the nonprostaglandin vasodilator sodium nitroprusside (SNP) and vasoconstrictor norepinephrine (NE) during 35% and 3% O 2 ventilation. Pulmonary vascular resistance was divided into arterial, middle (Rm), and venous segmental resistances in 20 isolated left lower canine lobes using a stop-flow technique. Pulmonary vascular resistance was also analyzed as the slope and intercept (P CRIT) of the pressure-flow relationship. We found that only PGI 2 specifically prevented the increase in Rm and P CRIT due to hypoxia. Sodium nitro prusside predominantly decreased venous segment resistance and, even in the presence of SNP, hypoxia significantly ( P < .05) increased Rm (0.0179 ± 0.0075 cm H 2O/mL/min) compared with control ventilation (0.0078 ± 0.0043 cm H 2O/mL/min). Both PGE 2 and NE increased PVR primarily by increasing the venous segmental resistance. After the addition of PGE 2 or NE, hypoxic ventilation did not result in further increases of Rm or P CRIT. We conclude that PGI 2 but not SNP selectively inhibits HPV and that neither PGE 2 nor NE further augment HPV. The direct effect of these drugs on the pulmonary circulation and their resultant changes in systemic oxygen delivery must be considered prior to their use in the clinical setting.