To determine whether the pulmonary and circulatory effects of intravenous Prostaglandins F2α and E2 are altered in the presence of emphysema and/or hypoxia, 19 New Zealand White rabbits were treated with 3 doses of intratracheal porcine pancreatic elastase (100 U/kg) administered at 4 day intervals to induce panacinar emphysema, and 19 were treated on a similar schedule with saline to serve as controls. Thirty days after their last elastase or saline treatment, rabbits were divided randomly into hypoxic and non-hypoxic breathing subgroups, so that there were 4 experimental groups: control/non-hypoxic (n=10), control/hypoxic (n=9), elastase/non-hypoxic (n=11), and elastase/hypoxic (n=8). All rabbits underwent pulmonary physiologic studies and received rapid intravenous infusions of PGF2α (6, 12, 14 μg) and PGE2 (1,3,6 μg). Lung resistance (RL), dynamic lung compliance (Cdyn), right ventricular systolic pressure (Prv), and mean aortic pressure (Paorta) were measured before, and 1 and 5 min. after prostaglandin infusions. At the conclusion of these studies, all rabbits were killed for morphometric and light microscopic analysis of their lungs. Elastase treated rabbits had physiologic, morphometric, and light microscopic evidence of panacinar emphysema. In the control/non-hypoxic group, PGF2α had no effect on Cdyn, but produced a decline in Paorta and an increase in RL and Prv after the 24 μg dose. In the same group, PGE2 had no effect on RL or Cdyn, but a decrease in Paorta was observed with all 3 doses. In addition, Prv increased after 6 μg of PGE2. These effects were produced by doses of PGF2α and PGE2 which were 12 and 3 times greater respectively than effects of similar magnitude in dogs. Except for the absence of an increase in RL after PGF2α 24 μg, the presence of emphysema did not alter the effects of PGF2α or PGE2. However, hypoxia irrespective of emphysema produced greater physiologic effects from both prostanoids. These findings indicate that rabbits are more resistant to the effects of PGE2 on pulmonary mechanics, and pulmonary and systemic vascular pressures. Furthermore, they suggest that hypoxia is a more important factor influencing pulmonary prostaglandin catabolism than anatomic pulmonary emphysema.
|Original language||English (US)|
|Number of pages||19|
|Journal||Research Communications in Chemical Pathology and Pharmacology|
|State||Published - Jan 1 1988|
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Pharmacology, Toxicology and Pharmaceutics(all)