Respiration and blood gases in the duck exposed to normocapnic and hypercapnic hypoxia.
Cardio-respiratory parameters were measured in the unrestrained, unanesthetized duck by whole body plethysmography during exposure to varied levels of inspired hypoxia without or with (3.7%) CO2. At any level of inspired PO2 (PIO2), ventilation (VE) was larger with CO2 inhalation, leading, for PIO2 greater than 50 Torr, to higher levels of arterial PO2 (PaO2) and O2 content (CaO2). Below PIO2 of 50 Torr, the (PI-Pa)O2 difference without CO2 reached a value as low as 5 Torr which was not diminished by further stimulation of VE by inhaled CO2. Without CO2 inhalation at this deep hypoxic level the ensuing hypoxia-induced respiratory alkalosis was partly compensated by lactacidosis, whereas CO2 inhalation resulted in markedly lower blood pH leading to significantly lower arterial and venous O2 content (Bohr effect). As a result, the deepest level of hypoxia tolerated without CO2 inhalation, 30 Torr, is significantly deeper than that, 36 Torr, tolerated when CO2 is inhaled. The data suggest that a number of factors contribute to the high hypoxia tolerance in birds, e.g. the effectiveness of parabronchial ventilation and the tolerance of low arterial PCO2 levels, whereby part of the lactacidosis is compensated.
D000136:Acid-Base Equilibrium; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood*; D002302:Cardiac Output; D004372:Ducks / Q000378:metabolism / Q000502:physiology*; D006935:Hypercapnia / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D000860:Hypoxia / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood*; D012119:Respiration
D002245:Carbon Dioxide; D010100:Oxygen