Department of Bioengineering, University of California, San Diego, La Jolla, California 92093-0412, USA.
Anesthesiology. 2011 Apr;114(4):901-11. doi: 10.1097/ALN.0b013e31820efb36.
To avoid unnecessary blood transfusions, physiologic transfusion triggers, rather than exclusively hemoglobin-based transfusion triggers, have been suggested. The objective of this study was to determine systemic and microvascular effects of using a perfluorocarbon-based oxygen carrier (PFCOC) to maintain perfusion and oxygenation during extreme anemia.
The hamster (weight, 55-65 g) window chamber model was used. Two isovolemic hemodilution steps were performed using hydroxyethyl starch, 10%, at normoxic conditions to a hematocrit of 19% (hemoglobin, 5.5 g/dl), the point at which the transfusion trigger was reached. Two additional hemodilution exchanges using the PFCOC (Oxycyte) and increasing the fraction of inspired oxygen to 1.0 were performed to reduce the hematocrit to 11% (hemoglobin, 3.8 g/dl) and 6% (hemoglobin, 2.0 g/dl), respectively. No control group was used in the study because this concentration of hemodilution is lethal with conventional plasma expanders. Systemic parameters, microvascular perfusion, functional capillary density, and oxygen tensions across the microvascular network were measured.
At 6% hematocrit, the PFCOC maintained mean arterial pressure, cardiac output, systemic oxygen delivery, and oxygen consumption. As hematocrit was decreased from 11% to 6%, functional capillary density, calculated microvascular oxygen delivery, and oxygen consumption decreased; and the oxygen extraction ratio was close to 100%. Peripheral tissue oxygenation was not predicted by systemic oxygenation.
The PFCOC, in conjunction with hyperoxia, was able to sustain organ function and partially provide systemic oxygenation during extreme anemia during the observation period. The PFCOC can work as a bridge until erythrocytes are available for transfusion or when additional oxygen is required, despite the possible limitations in peripheral tissue oxygenation.
为了避免不必要的输血，建议使用生理输血触发因素，而不仅仅是基于血红蛋白的输血触发因素。本研究的目的是确定使用全氟化碳基氧载体（PFCOC）在极度贫血期间维持灌注和氧合的全身和微血管效应。
使用仓鼠（体重 55-65 克）窗室模型。在常氧条件下，使用 10%羟乙基淀粉进行两次等容血液稀释步骤，使血细胞比容降至 19%（血红蛋白 5.5 g/dl），达到输血触发点。然后使用 PFCOC（Oxycyte）进行另外两次血液稀释交换，并将吸入氧分数增加到 1.0，将血细胞比容分别降至 11%（血红蛋白 3.8 g/dl）和 6%（血红蛋白 2.0 g/dl）。由于这种程度的血液稀释用常规血浆扩容剂是致命的，因此本研究未使用对照组。测量全身参数、微血管灌注、功能性毛细血管密度和微血管网络的氧分压。
在 6%的血细胞比容下，PFCOC 维持平均动脉压、心输出量、全身氧输送和氧消耗。随着血细胞比容从 11%降至 6%，功能性毛细血管密度、计算的微血管氧输送和氧消耗降低；氧提取率接近 100%。外周组织氧合不能通过全身氧合来预测。
PFCOC 与高氧结合，能够在观察期间维持器官功能，并在极度贫血期间部分提供全身氧合。尽管外周组织氧合可能存在限制，但 PFCOC 可以作为桥梁，直到红细胞可用于输血或需要额外的氧气。
