Effects of Chronic Hyperoxia on the Cardiovascular Responses to Vasoative Compounds in the Rabbit.
Abstract
Hyperoxia has been shown to disrupt certain membrane bound enzyme systems within the pulmonary endothelium which are responsible for the metabolsim of several endogeneous vasoactive compounds. This study evaluated whether the potential disruption of the angiotensin converting enzyme (ACE) and the prostaglandin dehydrogenase/reductase (PGDH/R) enzyme, as a consequence of chronic hyperoxia, would alter the activation/deactivation of the angiotensins (I and Ii) or prostaglandins and thereby alter their peripheral cardiovascular actions. Two groups of conscious, chronically catheterized rabbits, one group exposed to ambient air and the other group exposed to > 98% oxygen, were given bolus injections of angiotensin I, angiotensin II, prostaglandin E sub 2 sodium nitroprusside, and phenylephrine before and during extended exposure to air or oxygen. Basal mean arterial pressure decreased for both groups during the exposure. However, the normoxic and the hyperoxic basal mean arterial pressures were never significantly different from one another at any exposure point. Basal heart rate for the hyperoxic animals significantly increased during the exposure period while the basal heart rate for the normoxic group was unaltered.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 1985
- Accession Number
- ADA156968
Entities
People
- J. C. Sventek
Organizations
- Air Force Institute of Technology