In the anesthetised dog an infusion of exogenous prostaglandin E1 (100μG/min) inhibits the pulmonary vascular pressor response to hypoxia. Both 25 and 100 μG/min PGE1 can reduce the transient pulmonary hypertension caused by a bolus of prostaglandin F2α. This suggests that hypoxia and PGF2α may share a final common pathway in producing pulmonary vasoconstriction. These results may help to explain the mechanism by which endotoxin inhibits the pulmonary vascular response to hypoxia. This effect is probably achieved by stimulating the production of an endogenous dilator prostaglandin. Exogenous PGE1 can mimic this effect.
Bibliographical noteFunding Information:
This work was supported by grants #HL 14985 and HL 05973 from the National Institutes of Health. Dr. Weir is the recipient of a Fulbright Scholarship. Dr. Grover is the recipient of an NIH Research Career Development Award #HL 29237. We are grateful for the assistance of R. Glas, B. Kaplan, M. Munroe, D. Smith, E. Toyos, S. Hofmeister and D. Jackson. Prostaglandins E 1 and F2~ were kindly provided by the Upjohn Company.