Deem S, Alberts M K, Bishop M J, Bidani A, Swenson E R
Department of Anesthesiology, University of Washington, Seattle, 98195, USA.
J Appl Physiol (1985). 1997 Jul;83(1):240-6. doi: 10.1152/jappl.1997.83.1.240.
Isovolemic hemodilution does not appear to impair CO2 elimination nor cause CO2 retention despite the important role of red blood cells in blood CO2 transport. We studied this phenomenon and its physiological basis in eight New Zealand White rabbits that were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Isovolemic anemia was induced by simultaneous blood withdrawal and infusion of 6% hetastarch in sequential stages; exchange transfusions ranged from 15-30 ml in volume. Variables measured after each hemodilution included hematocrit (Hct), arterial and venous blood gases, mixed expired PCO2 and PO2, and blood pressure; also, O2 consumption, CO2 production, cardiac output (Q), and physiological dead space were calculated. Data were analyzed by comparison of changes in variables with changes in Hct and by using the model of capillary gas exchange described by Bidani (J. Appl. Physiol. 70: 1686-1699, 1991). There was complete compensation for anemia with stability of venous and arterial PCO2 between Hct values of 36 +/- 3 and 12 +/- 1%, which was predicted by the mathematical model. Over this range of hemodilution, Q rose 50%, and the O2 extraction ratio increased 61% without a decline in CO2 production or a rise in alveolar ventilation. The dominant compensations maintaining CO2 transport in normovolemic anemia include an increased Q and an augmented Haldane effect arising from the accompanying greater O2 extraction.
尽管红细胞在血液二氧化碳运输中起重要作用，但等容血液稀释似乎不会损害二氧化碳的排出，也不会导致二氧化碳潴留。我们在8只新西兰白兔身上研究了这一现象及其生理基础，这些兔子被麻醉、麻痹并以固定的分钟通气量进行机械通气。通过依次同时抽血和输注6%羟乙基淀粉诱导等容性贫血；换血量为15 - 30毫升。每次血液稀释后测量的变量包括血细胞比容（Hct）、动脉和静脉血气、混合呼出的PCO₂和PO₂以及血压；此外，还计算了氧耗量、二氧化碳产生量、心输出量（Q）和生理死腔。通过比较变量变化与Hct变化，并使用Bidani（《应用生理学杂志》70: 1686 - 1699, 1991）描述的毛细血管气体交换模型对数据进行分析。在血细胞比容值为36±3%至12±1%之间，静脉和动脉PCO₂稳定，贫血得到完全代偿，这是数学模型所预测的。在这个血液稀释范围内，心输出量增加50%，氧摄取率增加61%，而二氧化碳产生量没有下降，肺泡通气量也没有增加。在等容性贫血中维持二氧化碳运输的主要代偿机制包括心输出量增加以及伴随更大的氧摄取而产生的增强的哈代效应。
