Abstract
Vascular endothelial cells produce or metabolize vasoactive substances, which regulate or modulate vascular tone. A potent vasodilator, prostaglandin I2 (PGI2) is known to be released from vascular endothelium in increased quantities in response to not only various chemical stimuli but also mechanical stimuli such as a increased blood flow. We performed this study to know whether pulmonary hemodynamic forces would affect lung PGI2 production and PGI2 acts on pulmonary vessels to maintain a low resistance in the pulmonary circulation. We measured plasma 6-keto-PGF1α, the metabolite of PGI2, during pulmonary blood flow alterations in rabbits.
The alterations were made by unilateral complete pneumothorax or pulmonary artery occulusion, which decreased pulmonary vascular bed and increased blood flow in the redisual pulmonary vessels. Plasma 6-keto-PGF1α level increased during such procedures but the rise of pulmonary arterial pressure was small and transient. Cyclooxygenase inhibition did not affect the change of pulmonary arterial pressure during pulmonary artery occulusion.
These data suggest that PGI2 is produced by pulmonary vessels in response to the increased blood flow but it may not participate in modulation of pulmonary hemodynamics.
