Shams H, Scheid P
Respir Physiol. 1987 Jan;67(1):1-12. doi: 10.1016/0034-5687(87)90002-8.
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.
在未束缚、未麻醉的鸭身上，通过全身体积描记法测量心肺参数，测量过程中使其暴露于不同水平的吸入性低氧环境，分为无二氧化碳和有（3.7%）二氧化碳两种情况。在任何吸入氧分压（PIO2）水平下，吸入二氧化碳时的通气量（VE）更大，当PIO2大于50托时，会导致动脉血氧分压（PaO2）和氧含量（CaO2）升高。在PIO2低于50托时，无二氧化碳时的（PI - Pa）O2差值低至5托，吸入二氧化碳进一步刺激VE也不会使其减小。在这种深度低氧水平下，不吸入二氧化碳时，随之而来的低氧诱导的呼吸性碱中毒部分被乳酸性酸中毒代偿，而吸入二氧化碳则导致血液pH值显著降低，进而导致动脉和静脉氧含量显著降低（波尔效应）。结果，不吸入二氧化碳时所能耐受的最深低氧水平为30托，显著低于吸入二氧化碳时所能耐受的36托。数据表明，多种因素导致鸟类具有较高的低氧耐受性，例如副支气管通气的有效性以及对低动脉血二氧化碳水平的耐受性，其中部分乳酸性酸中毒得到了代偿。
