Blood-gas transport in awake rabbits exposed to normobaric hyperoxia.
The time course and terminal effects of normobaric oxygen exposure on the gas transport chain were studied in awake, catheterized rabbits exposed to air (n = 8) for 96 h or 100% O2 (n = 10) until death. O2-breathing animals survived 60.2 (+/- 13.5 SD) h. Pao2 increased and was maintained until within 4.9 (+/- 1.4) h of death. Mixed venous O2 tension rose sharply but transiently upon O2 exposure. In most animals, death followed a precipitous fall in PaCO2, a moderate rise in PaCO2, and a drop in pHa. The terminal acidosis was largely metabolic, nearly half due to lactic acidemia. There were transient appearances of metabolic acids early in the exposures before the PaCO2 decreased. Furthermore, in the last hours, fixed acids appeared when PaCO2 was unchanged or slightly decreased, but before the animal became hypoxemic. Metabolic acidosis without arterial hypoxemia could result from cardiac insufficiency, or alterations in metabolism, or in patterns of distribution of blood flow within peripheral beds. Thus, normobaric O2 exposure has precipitous and terminal effects on pulmonary gas exchange, but arterial hypoxemia is not necessarily the cause of death.
D000136:Acid-Base Equilibrium; D000399:Air Pressure; D000818:Animals; D001274:Atmospheric Pressure; D001692:Biological Transport; D002245:Carbon Dioxide / Q000097:blood; D007700:Kinetics; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D010100:Oxygen / Q000008:administration & dosage / Q000097:blood*; D011817:Rabbits
D007773:Lactates; D002245:Carbon Dioxide; D019344:Lactic Acid; D010100:Oxygen