The benefits of remote ischaemic conditioning (RIC) have been difficult to translate to humans, when considering traditional outcome measures, such as mortality and heart failure. This paper reviews the recent literature of the anti-inflammatory effects of RIC, with a particular focus on the innate immune response and cytokine inhibition. Given the current COVID-19 pandemic, the inflammatory hypothesis of cardiac protection is an attractive target on which to re-purpose such novel therapies. A PubMed/MEDLINE™ search was performed on July 13th 2020, for the key terms RIC, cytokines, the innate immune system and inflammation. Data suggest that RIC attenuates inflammation in animals by immune conditioning, cytokine inhibition, cell survival and the release of anti-inflammatory exosomes. It is proposed that RIC inhibits cytokine release via a reduction in nuclear factor kappa beta (NF-κB)-mediated NLRP3 inflammasome production. In vivo, RIC attenuates pro-inflammatory cytokine release in myocardial/cerebral infarction and LPS models of endotoxaemia. In the latter group, cytokine inhibition is associated with a profound survival benefit. Further clinical trials should establish whether the benefits of RIC in inflammation can be observed in humans. Moreover, we must consider whether uncomplicated MI and elective surgery are the most suitable clinical conditions in which to test this hypothesis.

考虑到死亡率和心力衰竭等传统结果指标时，远程缺血调理 (RIC) 的益处难以转化为人类。本文回顾了最近关于 RIC 抗炎作用的文献，特别关注先天免疫反应和细胞因子抑制。鉴于当前的 COVID-19 大流行，心脏保护的炎症假说是重新利用这种新疗法的一个有吸引力的目标。2020 年 7 月 13 日进行了 PubMed/MEDLINE™ 搜索，检索关键术语 RIC、细胞因子、先天免疫系统和炎症。数据表明，RIC 通过免疫调节、细胞因子抑制、细胞存活和抗炎外泌体的释放来减轻动物的炎症。建议 RIC 通过减少核因子 kappa β (NF-κB) 介导的 NLRP3 炎性体产生来抑制细胞因子释放。在体内，RIC 可减弱心肌/脑梗塞和内毒素血症 LPS 模型中促炎细胞因子的释放。在后一组中，细胞因子抑制与显着的生存益处相关。进一步的临床试验应确定 RIC 在炎症中的益处是否可以在人类中观察到。此外，我们必须考虑单纯性心肌梗死和择期手术是否是检验这一假设的最合适的临床条件。细胞因子抑制与显着的生存益处相关。进一步的临床试验应确定 RIC 在炎症中的益处是否可以在人类中观察到。此外，我们必须考虑单纯性心肌梗死和择期手术是否是检验这一假设的最合适的临床条件。细胞因子抑制与显着的生存益处相关。进一步的临床试验应确定 RIC 在炎症中的益处是否可以在人类中观察到。此外，我们必须考虑单纯性心肌梗死和择期手术是否是检验这一假设的最合适的临床条件。