Abstract
Preadaptation of adult rats to hypoxia (10% O2 for 5 days) results in tolerance to oxygen-induced lung injury (greater than 95% O2 for 2 days). This study investigated whether hypoxia preadaptation maintained an endothelial cell metabolic function, angiotensin-converting enzyme (ACE) activity, despite exposure to hyperoxia. Lung ACE activity was measured as the capacity of isolated, ventilated, perfused lungs to hydrolyze an ACE substrate, benzoyl-phenylalanyl-alanyl-proline (BPAP), after in vivo hypoxia, hyperoxia, or sequential hypoxia-hyperoxia exposure. The results indicated that (1) hyperoxia decreases BPAP hydrolysis in isolated lungs, (2) hypoxia preadaptation does not affect BPAP hydrolysis (measured at ambient PO2), and (3) hypoxia preadaptation prevents hyperoxia-induced depression of lung ACE activity. These data imply that lung microvascular endothelial cells participate in the development of oxygen tolerance in this model.
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