Pulmonary prostacyclin production with increased flow and sympathetic stimulation

Abstract

We evaluated the effects of an abrupt increase in flow and of a subsequent sympathetic nerve stimulation on the pulmonary production of prostacyclin (PGI2) and thromboxane A2 (TXA2) in canine isolated left lower lobes perfused in situ with pulsatile flow. When flow was abruptly increased from 50 +/- 3 to 288 +/- 2 ml/min, mean pulmonary arterial pressure (Ppa) increased by 15 +/- 2 Torr and then declined by 2.4 Torr over the next 5 min. This secondary decrease in Ppa was associated with a significant 0.26 +/- 0.11 ng/ml increase in the pulmonary venous concentration of the stable PGI2 hydrolysis product 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) as determined by radioimmunoassay. Stimulation of the left stellate ganglion usually resulted in an increase in Ppa which peaked at 1.1 +/- 0.6 Torr above its prestimulus level and then declined over the next 5 min. Associated with this decline was a 0.24 +/- 0.11 ng/ml increase in 6-keto-PGF1 alpha at 1 min. We suggest that the decline in Ppa is due to the synthesis and release of PGI2 by the endothelial cells in response to an increase in perfusion pressure.

Why is functional capacity decreased in hypertensive patients? From mechanisms to clinical studies

“…56,57 These results could be explained by abnormalities in the number of adrenergic receptors in pulmonary circulation, or their quality. 58 The other explanation could lie in the interconnections between Na þ , Ca 2þ , and natriuretic peptides, biohumoral systems involved in the smooth muscle excitation and contraction. 55,59 Additional factors that contribute to impaired pulmonary resistance are certainly oxidative stress products, which cause endothelial damage and induce vasoconstriction, as well as vasoconstrictors endothelin-1 and angiotensin II, and vasodilators such as prostacyclin and nitric oxide, which are normally released by pulmonary endothelium.…”

NO and prostaglandin interactions during hemodynamic stress in the fetal ovine pulmonary circulation

“…Previous studies that have examined the roles of NO and PGs in modulating the response to shear stress in the postnatal circulation are conflicting. Abrupt increases in flow stimulate both NO and PG release in isolated endothelial cells in culture (5,8,11,13,24,32). In isolated neonatal lamb lungs, NOS inhibition during normoxia increased PVR more than COX inhibition, but during hypoxia, COX inhibition augmented PVR more than NOS inhibition (15).…”

Cyclooxygenase Inhibition Potentiates the Pulmonary Vascular Responses to Ethanol in Dogs

“…A second hypothesis to explain the increase in vascular tone after cyclooxygenase inhibition is related to a di minished production of the vasodilator pros tanoid, prostacyclin (PGI2). Several investi gators [21][22][23] suggested that PGI2 appears to be the principle cyclooxygenase product in dog lung and may be important for main tenance of low pulmonary vascular resis tance. As such, it seems that cyclooxygenase inhibition increases pulmonary vascular tone by reducing the production of vasodila tor prostaglandins, with PGI2 the most likely candidate.…”