Effects of Chronic Hyperoxia on the Cardiovascular Responses to Vasoative Compounds in the Rabbit.
AIR FORCE INST OF TECH WRIGHT-PATTERSON AFB OH
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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 dehydrogenasereductase PGDHR enzyme, as a consequence of chronic hyperoxia, would alter the activationdeactivation 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.
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