The effects of hyperoxia on oxygen uptake during acute anemia.
The effects of normobaric hyperoxia on the oxygen uptake (VO2) and cardiovascular responses of the whole body and hindlimb during anemia were investigated. Anesthetized, paralyzed dogs were ventilated for 20-min periods with room air (normoxia), 100% O2 (hyperoxia), and returned to room air. Anemia (hematocrit = 15%) was then induced by isovolemic dextran-for-blood exchange and the normoxia, hyperoxia, normoxia sequence was repeated. Whole body VO2 and cardiac output rose following anemia, and then fell (p less than 0.05) with hyperoxia during anemia. These responses were not abolished by beta-blockade with propranolol (1 mg/kg, iv) or bilateral vagotomy. The hindlimb data for blood flow and VO2 were similar in direction to those of the whole body but were more variable. Section of the sciatic and femoral nerves did not appear to have significant effect on the limb responses to hyperoxia. The decrease in whole body and hindlimb VO2 with hyperoxia during anemia may have resulted from a redistribution of capillary blood flow away from exchange vessels in response to the elevated PO2.
D000208:Acute Disease; D000740:Anemia / Q000378:metabolism*; D000818:Animals; D002302:Cardiac Output; D004285:Dogs; D005121:Extremities / Q000098:blood supply / Q000378:metabolism; D005260:Female; D006339:Heart Rate; D006400:Hematocrit; D008297:Male; D010100:Oxygen / Q000097:blood / Q000494:pharmacology*; D010101:Oxygen Consumption
D010100:Oxygen