Kinetic analyses of the effects of hyperoxia and hypoxia on vascular cyclooxygenase activity in vitro.
Kinetic analyses were performed to understand the mechanism of hyperoxic induced inhibition of prostacyclin synthesis by human umbilical arteries. Brief exposure of arterial segments to oxygen resulted in over 30% decrease in Vmax of cyclooxygenase in treated vessels. In contrast, cyclooxygenase from hypoxic arterial segments showed approximately a 49% increase in Vmax. There were no significant differences in apparent Km values. These studies suggest that the decreased production of prostacyclin by hyperoxic tissue is due to cyclooxygenase inactivation.
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D006801:Humans; D006931:Hyperbaric Oxygenation; D000860:Hypoxia / Q000201:enzymology*; D007231:Infant, Newborn; D007700:Kinetics; D008861:Microsomes / Q000201:enzymology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D013997:Time Factors; D014469:Umbilical Arteries / Q000378:metabolism*
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D011451:Prostaglandin-Endoperoxide Synthases