Prostaglandins and Vasoactive Lung Peptides Released from the Lungs During Experimental Pulmonary Edema
1978 Volume 16 Issue 4 Pages 247-254
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1978 Volume 16 Issue 4 Pages 247-254
Pulmonary edema was induced in isolated, perfused cat lung by raising outflow pressure. Samples of perfusate and foam during pulmonary edema were collected for measuring the levels of protaglandins (PGF2α, PG E) and vasoactive lung peptides (VLP) by a radioimmunoassay. In additon, the effects of PG F2α, PG E2 and VLP on the pulmonary and systemic circulation and airway were studied in anesthetized cats and dogs.
1) PG F2α and PG E increased significantly in edema foam but in perfusate during pulmonary edema, did not significantly change. The increase of PG F2α in foam was remarkably.
In intact cats, PG F2α increased significantly pulmonary arterial pressure and airway pressure whereas cardiac output and systemic arterial pressure were significantly decreased. PG E2 resulted in a significant increase in pulmonary arterial pressue but in a significant decrease in systemic arterial pressure whereas cardiac output was not altered. These results indicated that both of PG F2α and PG E2 caused pulmonary vasoconstriction.
2) VLP increased in foam during pulmonary edema. This VLP has not been extracted and purified completely yet but has been found to contain at least two active principles, one of which relaxed and the other contracted isolated smooth-muscle organs.
Both pulmonary peptide fructions induced systemic vasodilation, evidenced by an increase in femoral blood flow with a fall of systemic blood pressure. But in pulmonary circulation, the isolated pulmonary vascular smooth-muscle actions of these two peptides suggested that one peptide (spasmogenic) induced pulmonary vasoconstriciton and other (relaxant) caused pulmonary vasodilation. Particularly, the smooth-muscle action of spasmogenic VLP mimiced these of the prostaglandins and prostaglandin-related compounents.
The above biological activities of PGs and VLP, which were demonstrated in foam during pulmonary edema, suggest that pulmonary edema may be caused by these vasoactive substances and moreover, these vasoactive substances may contribute to the production of bronchoconstriction, systemic hypotension and pulmonary hypertension during pulmonary edema.
