Malmberg P O, Woodson R D
J Appl Physiol Respir Environ Exerc Physiol. 1979 Oct;47(4):882-8. doi: 10.1152/jappl.1979.47.4.882.
Effect of anemia on tolerance of hemorrhagic shock in rats was studied to examine opposing effects of altered oxygen capacity and viscosity on oxygen delivery at reduced blood flow. Hematocrit was first reduced by exchange transfusion. Hypotension (BP = 30 Torr) was induced and maintained at this level by controlled hemorrhage; it was terminated when reinfusion of shed blood became necessary to sustain this blood pressure. The period of compensation (time at 30 Torr until reinfusion) in control rats (Hct = 42.5 +/- 2.7%) was 59.23 min; in anemic rats (Hct = 23.3 +/- 2.2%) it was 53 +/- 15 min (SD, P = 0.086). Bleeding rate during shock, mortality, VO2, acid-base balance, and mortality were not influenced by anemia, except for slightly higher lactate in late shock in anemia. The lack of influence of anemia (cf. other perturbations of oxygen transport) was apparently due to a 59-88% increase in cardiac ouput during shock in anemia, which maintained VO2.
研究了贫血对大鼠失血性休克耐受性的影响,以检验氧容量和粘度改变对血流减少时氧输送的相反作用。首先通过换血降低血细胞比容。通过控制性出血诱导低血压(血压 = 30 托)并维持在该水平;当为维持该血压而必须回输流出的血液时终止实验。对照大鼠(血细胞比容 = 42.5 ± 2.7%)的代偿期(血压 30 托直至回输的时间)为 59.23 分钟;贫血大鼠(血细胞比容 = 23.3 ± 2.2%)的代偿期为 53 ± 15 分钟(标准差,P = 0.086)。除贫血大鼠休克后期乳酸略高外,休克期间的出血率、死亡率、耗氧量、酸碱平衡和死亡率均不受贫血影响。贫血缺乏影响(与其他氧运输紊乱情况相比)显然是由于贫血大鼠休克期间心输出量增加了 59 - 88%,从而维持了耗氧量。