Marini C P, Russo G C, Nathan I M, Jurkiewicz A, McNelis J
Long Island Jewish Medical Center, Department of Surgery, Section of Critical Care, New Hyde Park, New York, USA.
Am J Surg. 2000 Aug;180(2):108-14. doi: 10.1016/s0002-9610(00)00424-4.
The purpose of this prospective, randomized, controlled study was to investigate the effects of hematocrit (Hct) on regional oxygen delivery and extraction following induction of adult respiratory distress syndrome (ARDS) in an animal model.
Animals were instrumented to monitor central venous pressure (CVP), systemic mean arterial pressure (MAP), pulmonary artery occlusion pressure (PAOP), and cardiac output (CO) and to measure blood flow in the renal, hepatic, and superior mesenteric arteries and portal vein. ARDS was induced, positive end expiratory pressure (PEEP) applied and CO was maximized with volume loading and epinephrine infusion. Data were acquired at baseline (BL) and at Hct levels ranging from 25% to 50%.
Systemic DO(2) increased steadily and significantly with increased Hct. Systemic O(2) extraction ratio (O(2)ER) decreased significantly with increasing Hct until a threshold value of 40%, after which further increases in Hct did not cause a statistically significant decrease in O(2)ER. Similarly, renal and hepatic DO(2) increased and O(2)ER decreased in a statistical significant manner with transfusions up to a Hct of 35%. In the splanchnic circulation blood transfusions did not cause any statistically significant increase in DO(2), and O(2)ER showed no decrease after an Hct of 35%. Systemic, renal, hepatic, and splanchnic VO(2) were not affected by changes in Hct. Blood viscosity decreased from a baseline value of 2.9+/-0.2 centipoise at a Hct of 38% to 2.3+/-0.1 centipoise at a Hct of 25% (P<0.05). Viscosity increased progressively with increasing hematocrits and reached the value of 4.2+/-0.2 centipoise at an Hct of 50% (P<0.05 versus Hct 30%, 35%, 40%, 45%).
Based on the results of this non-supply-dependent animal model we conclude that a progressive increase in Hct up to 40% causes a corresponding increase in systemic DO(2) associated with a decrease in O(2)ER. However, there is no improvement in renal, hepatic, and splanchnic DO(2) and O(2)ER after a threshold Hct of 35%. All other factors being the same, an Hct greater than 35% may in fact cause a decrease in blood flow rate and change in blood flow characteristics as a consequence of increased blood kinematic viscosity, which may alter and compromise cellular oxygen transfer.
本前瞻性、随机、对照研究的目的是在动物模型中研究血细胞比容（Hct）对成人呼吸窘迫综合征（ARDS）诱导后局部氧输送和摄取的影响。
对动物进行仪器监测，以测量中心静脉压（CVP）、体循环平均动脉压（MAP）、肺动脉闭塞压（PAOP）和心输出量（CO），并测量肾、肝和肠系膜上动脉及门静脉的血流。诱导ARDS，应用呼气末正压（PEEP），并通过容量负荷和肾上腺素输注使CO最大化。在基线（BL）以及Hct水平为25%至50%时采集数据。
随着Hct升高，体循环氧输送（DO₂）稳步且显著增加。随着Hct升高，体循环氧摄取率（O₂ER）显著降低，直至阈值40%，此后Hct进一步升高未导致O₂ER出现统计学显著降低。同样，输血使Hct达到35%之前，肾和肝的DO₂增加，O₂ER以统计学显著方式降低。在内脏循环中，输血未使DO₂出现任何统计学显著增加，且Hct达到35%后O₂ER未降低。体循环、肾、肝和内脏的氧耗（VO₂）不受Hct变化影响。血液黏度从Hct为38%时的基线值2.9±0.2厘泊降至Hct为25%时的2.3±0.1厘泊（P<0.05）。随着血细胞比容升高，黏度逐渐增加，在Hct为50%时达到4.2±0.2厘泊（与Hct 30%、35%、40%、45%相比，P<0.05）。
基于这个非供应依赖型动物模型的结果，我们得出结论，Hct逐渐升高至40%会导致体循环DO₂相应增加，同时O₂ER降低。然而，Hct超过35%的阈值后，肾、肝和内脏的DO₂及O₂ER并无改善。在所有其他因素相同的情况下，Hct大于35%实际上可能由于血液运动黏度增加导致血流速度降低以及血流特性改变，这可能会改变并损害细胞氧转运。
