Departments of Hand and Plastic Surgery and Intensive Care, Burn Center, Linköping County Council, Linköping, Sweden; Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
J Intern Med. 2013 Dec;274(6):505-28. doi: 10.1111/joim.12139.
Oxygen treatment has been a cornerstone of acute medical care for numerous pathological states. Initially, this was supported by the assumed need to avoid hypoxaemia and tissue hypoxia. Most acute treatment algorithms, therefore, recommended the liberal use of a high fraction of inspired oxygen, often without first confirming the presence of a hypoxic insult. However, recent physiological research has underlined the vasoconstrictor effects of hyperoxia on normal vasculature and, consequently, the risk of significant blood flow reduction to the at-risk tissue. Positive effects may be claimed simply by relief of an assumed local tissue hypoxia, such as in acute cardiovascular disease, brain ischaemia due to, for example, stroke or shock or carbon monoxide intoxication. However, in most situations, a generalized hypoxia is not the problem and a risk of negative hyperoxaemia-induced local vasoconstriction effects may instead be the reality. In preclinical studies, many important positive anti-inflammatory effects of both normobaric and hyperbaric oxygen have been repeatedly shown, often as surrogate end-points such as increases in gluthatione levels, reduced lipid peroxidation and neutrophil activation thus modifying ischaemia-reperfusion injury and also causing anti-apoptotic effects. However, in parallel, toxic effects of oxygen are also well known, including induced mucosal inflammation, pneumonitis and retrolental fibroplasia. Examining the available 'strong' clinical evidence, such as usually claimed for randomized controlled trials, few positive studies stand up to scrutiny and a number of trials have shown no effect or even been terminated early due to worse outcomes in the oxygen treatment arm. Recently, this has led to less aggressive approaches, even to not providing any supplemental oxygen, in several acute care settings, such as resuscitation of asphyxiated newborns, during acute myocardial infarction or after stroke or cardiac arrest. The safety of more advanced attempts to deliver increased oxygen levels to hypoxic or ischaemic tissues, such as with hyperbaric oxygen therapy, is therefore also being questioned. Here, we provide an overview of the present knowledge of the physiological effects of oxygen in relation to its therapeutic potential for different medical conditions, as well as considering the potential for harm. We conclude that the medical use of oxygen needs to be further examined in search of solid evidence of benefit in many of the current clinical settings in which it is routinely used.
氧疗一直是众多病理状态下急性医疗的基石。最初，这是基于避免低氧血症和组织缺氧的假设需要。因此，大多数急性治疗算法都推荐自由使用高分数的吸氧，通常在没有首先确认存在缺氧损伤的情况下。然而，最近的生理学研究强调了高氧对正常血管的血管收缩作用，因此，有风险的组织的血流显著减少。仅仅通过缓解假设的局部组织缺氧，就可以声称有积极的效果，例如在急性心血管疾病、由于中风或休克或一氧化碳中毒引起的脑缺血等情况下。然而，在大多数情况下，不是全身性缺氧而是高氧诱导的局部血管收缩作用的风险可能是现实的。在临床前研究中，多次反复显示了常氧和高压氧的许多重要的抗炎的积极作用，通常作为替代终点，如谷胱甘肽水平升高、脂质过氧化减少和中性粒细胞激活，从而改变缺血再灌注损伤，并引起抗凋亡作用。然而，同时，氧的毒性作用也广为人知，包括诱导的粘膜炎症、肺炎和视网膜后纤维增生。检查现有的“强有力”临床证据，如通常声称的随机对照试验，很少有阳性研究经得起仔细审查，一些试验表明没有效果，甚至因为氧疗组的结果更差而提前终止。最近，这导致了在一些急性治疗环境中采取不那么激进的方法，甚至不提供任何补充氧气，如窒息新生儿复苏、急性心肌梗死期间或中风或心脏骤停后。因此，对增加缺氧或缺血组织的氧水平的更先进的尝试，如高压氧治疗的安全性也受到质疑。在这里，我们提供了氧在不同医疗条件下的治疗潜力及其治疗潜力的生理效应的概述，同时考虑了潜在的危害。我们的结论是，需要进一步检查氧气的医疗用途，以寻找许多目前常规使用的临床环境中受益的可靠证据。
