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在成人呼吸窘迫综合征中,组织氧摄取的调节受到干扰。

Regulation of tissue oxygen extraction is disturbed in adult respiratory distress syndrome.

作者信息

Kariman K, Burns S R

出版信息

Am Rev Respir Dis. 1985 Jul;132(1):109-14. doi: 10.1164/arrd.1985.132.1.109.

Abstract

To test the hypothesis that regulation of tissue oxygen (O2) extraction is disturbed in adult respiratory distress syndrome (ARDS), the relationship between O2 availability and O2 extraction ratio (O2ER) was studied in 36 patients with pulmonary edema who met the criteria for either ARDS (n = 21) or acute congestive heart failure (CHF) (n = 15). We found that in response to changes in the levels of O2 availability there was a significantly (p = 0.01) greater negative correlation of change in O2ER for the CHF (r = -0.67) than for the ARDS group (r = -0.41). Whereas patients with CHF eventually died of pump failure and low O2 delivery, the ARDS group developed multiorgan failure, especially renal failure, despite significantly higher ratios of O2 availability to O2 consumption. These findings suggest that patients with ARDS have lost their ability to regulate their tissue O2 extraction to compensate for changes in the availability of O2 in order to meet demand. Pulmonary capillary endothelial injury, through its role on whole-body metabolism, may be responsible for this observation.

摘要

为验证成人呼吸窘迫综合征(ARDS)中组织氧(O₂)摄取调节受损这一假说,我们研究了36例符合ARDS(n = 21)或急性充血性心力衰竭(CHF)(n = 15)标准的肺水肿患者的氧供与氧摄取率(O₂ER)之间的关系。我们发现,对于氧供水平的变化,CHF组(r = -0.67)的O₂ER变化的负相关性显著(p = 0.01)大于ARDS组(r = -0.41)。尽管CHF患者最终死于泵衰竭和低氧输送,但ARDS组尽管氧供与氧消耗的比率显著更高,却出现了多器官衰竭,尤其是肾衰竭。这些发现表明,ARDS患者已丧失调节其组织氧摄取以补偿氧供变化以满足需求的能力。肺毛细血管内皮损伤通过其对全身代谢的作用,可能是造成这一现象的原因。

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