氧的输送和利用。

D R Dantzker
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引用次数: 0

摘要

在正常情况下,o2转运(TO 2 =心输出量x动脉o2含量)受到调节,以提供足够的o2来满足氧化磷酸化的需求,量化为o2消耗(VO 2)。当代谢需求增加时,TO 2增加,此外,组织对输送的o2的分数提取,o2er也增加,在最大VO 2时达到0.80的水平。如果TO 2减少,至少在实验动物中,最初可以通过增加o2er来维持VO 2,但最终该机制耗尽,VO 2开始下降,身体调用厌氧能量产生手段来维持细胞完整性。在正常人中,这个临界TO 2水平(TO 2crit)尚未确定,但在实验动物中,一旦O 2ER超过0.50,就会发现它。脓毒症和成人呼吸窘迫综合征的患者死亡率非常高,通常死于多器官衰竭。此外,他们在提取和利用输送的氧气的能力上也有明显的异常。尽管TO 2往往高于正常,但脓毒症患者通常有乳酸性酸中毒,当TO 2降低时,两组患者的O 2ER通常无法高于正常静息值0.33。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxygen delivery and utilization.

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)

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