Dantzker D R
Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, NY 11042.
Appl Cardiopulm Pathophysiol. 1991;3(4):345-50.
Under normal circumstances, O 2 transport (TO 2 = cardiac output x arterial O 2 content) is regulated to provide sufficient O 2 to meet the demands of oxidative phosphorylation, quantified as the O 2 consumption (VO 2). When metabolic demands increase, TO 2 is augmented and in addition, the fractional extraction of the delivered O 2 by the tissues, the O 2ER, also increases, to levels as high as 0.80 at maximum VO 2. If TO 2 is decreased, at least in the experimental animal, VO 2 can be maintained initially by an increase in O 2ER, but eventually this mechanism is exhausted, VO 2 begins to fall, and the body invokes anaerobic means of energy generation to maintain cell integrity. In normal man, this critical level of TO 2 (TO 2crit) has not been determined, but in experimental animals it has been found once the O 2ER exceeds 0.50. Patients with sepsis and the adult respiratory distress syndrome have a very high mortality and usually die as a result of multiple organ failure. They have in addition, an apparent abnormality in their ability to extract and utilize the delivered O 2. Despite a TO 2 which is often higher than normal, patients with sepsis commonly have a lactic acidosis and when TO 2 is reduced, both groups of patients are usually unable to increase their O 2ER above the normal resting value of 0.33.(ABSTRACT TRUNCATED AT 250 WORDS)
在正常情况下,氧气运输(TO₂ = 心输出量×动脉血氧含量)受到调节,以提供足够的氧气来满足氧化磷酸化的需求,氧化磷酸化的需求量以耗氧量(VO₂)来量化。当代谢需求增加时,TO₂会增加,此外,组织对输送来的氧气的分数提取量,即氧摄取率(O₂ER)也会增加,在最大VO₂时可高达0.80。如果TO₂降低,至少在实验动物中,VO₂最初可通过O₂ER的增加来维持,但最终这种机制会耗尽,VO₂开始下降,身体会调用无氧能量生成方式来维持细胞完整性。在正常人体中,尚未确定TO₂的这一临界水平(TO₂crit),但在实验动物中发现一旦O₂ER超过0.50就会出现。患有脓毒症和成人呼吸窘迫综合征的患者死亡率非常高,通常死于多器官功能衰竭。此外,他们在提取和利用输送来的氧气的能力方面存在明显异常。尽管脓毒症患者的TO₂通常高于正常水平,但他们通常会出现乳酸酸中毒,当TO₂降低时,这两组患者通常都无法将其O₂ER提高到正常静息值0.33以上。(摘要截选至250字)