Pape A, Meier J, Kertscho H, Steche M, Laout M, Schwerdel F, Wedel M, Zwissler B, Habler O
Johann Wolfgang Goethe-University, Frankfurt/Main, Germany.
Crit Care Med. 2006 May;34(5):1475-82. doi: 10.1097/01.CCM.0000215826.45839.36.
To investigate the impact of prophylactic hyperoxic ventilation with Fio2 0.6 on the physiologic limit of acute normovolemic anemia.
Prospective, controlled, randomized experimental study.
Experimental animal laboratory of a university hospital.
Fourteen anesthetized domestic pigs.
Animals were randomly ventilated with either Fio2 0.21 (group 0.21, n = 7) or Fio2 0.6 (group 0.6, n = 7), and acute anemia was induced by isovolemic blood-for-hydroxy-ethylstarch (HES) exchange using a 6% HES solution (130/0.4).
The blood-for-HES-exchange was continued until a sudden decrease of total body oxygen consumption indicated the onset of oxygen supply dependency (primary end point); the corresponding hemoglobin (Hb) concentration was defined as "critical" (Hb(crit)). Secondary end points were changes in myocardial function, central hemodynamics, oxygen transport, and tissue oxygenation. Compared with room air ventilation (Fio2 0.21), hyperoxic ventilation with Fio2 0.6 enabled a larger blood-for-HES-exchange (139%, 124/156) of circulating blood volume vs. 87% (68/94, p < .05), until Hb(crit) was reached (1.5 g/dL [1.4/2.1] vs. 2.4 g/dL [2.0/2.8], p < .05). At Hb 2.4 g/dL (i.e., Hb(crit) in group 0.21), animals of group 0.6 still presented with superior oxygen transport, tissue oxygenation, and hemodynamic stability. However, hemodynamic and oxygen transport variables were found deteriorated more severely at Hb 1.5 g/dL (i.e., Hb(crit) of group 0.6) compared with group 0.21 at Hb 2.4 g/dL.
During cell-free volume replacement, hyperoxic ventilation with Fio2 0.6 generates a readily usable plasmatic oxygen reserve and thereby increases the tolerance toward acute normovolemic anemia.
研究吸入氧分数（Fio2）为0.6的预防性高氧通气对急性等容性贫血生理极限的影响。
前瞻性、对照、随机实验研究。
大学医院的实验动物实验室。
14只麻醉的家猪。
动物随机接受Fio2为0.21（0.21组，n = 7）或Fio2为0.6（0.6组，n = 7）的通气，使用6%羟乙基淀粉（HES）溶液（130/0.4）通过等容血液-羟乙基淀粉交换诱导急性贫血。
血液-羟乙基淀粉交换持续进行，直至全身氧耗突然下降表明出现氧供依赖（主要终点）；相应的血红蛋白（Hb）浓度被定义为“临界值”（Hb(crit)）。次要终点为心肌功能、中心血流动力学、氧运输和组织氧合的变化。与室内空气通气（Fio2 0.21）相比，Fio2为0.6的高氧通气在达到Hb(crit)之前（1.5 g/dL [1.4/2.1] 对 2.4 g/dL [2.0/2.8]，p < 0.05），能使循环血容量进行更大程度的血液-羟乙基淀粉交换（139%，124/156），而室内空气通气组为87%（68/94，p < 0.05）。在Hb为2.4 g/dL时（即0.21组的Hb(crit)），0.6组动物仍表现出更好的氧运输、组织氧合和血流动力学稳定性。然而，与0.21组在Hb为2.4 g/dL时相比，在Hb为1.5 g/dL时（即0.6组的Hb(crit)），血流动力学和氧运输变量恶化更为严重。
在无细胞容量置换期间，Fio2为0.6的高氧通气可产生易于利用的血浆氧储备，从而提高对急性等容性贫血的耐受性。
