Arterial and tissue gas tensions in rats during development of pulmonary oxygen poisoning.
Oxygen and carbon dioxide tensions of arterial blood and subcutaneous tissue were studied in rats during 84 h of continuous exposure to oxygen. O2 and CO2 tensions in the subcutaneous tissue were measured by means of an implanted Silastic tonometer. As pulmonary edema developed after 48 h of exposure to oxygen, Pao2 started to decline and PaCO2 rose. Tissue Po2 decreased below the normal level already after 24 h of exposure, probably due to O2-induced vasoconstriction. After 84 h of oxygen exposure, the mean tissue Po2 was 29 mm Hg. In general, a distinctly hypoxic tissue microclimate was not observed. After 48 h of exposure to oxygen, the tissue PCO2 exceeded the control level. An 84-h exposure resulted in a profound retention of CO2, both in peripheral tissues and arterial blood. It is concluded that, in contrast to earlier suggestions, hypercapnia rather than hypoxia is the final factor leading to death in oxygen toxicity.
D000818:Animals; D001273:Atmosphere Exposure Chambers; D002245:Carbon Dioxide / Q000097:blood; D004780:Environment, Controlled; D004781:Environmental Exposure; D006801:Humans; D006935:Hypercapnia / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism; D010100:Oxygen / Q000097:blood / Q000633:toxicity*; D010101:Oxygen Consumption; D010313:Partial Pressure; D051381:Rats
D002245:Carbon Dioxide; D010100:Oxygen