首页> 外文期刊>Basic Research in Cardiology: Official Journal of the German Association of Cardiovascular Research >Pre- and postconditioning the heart with hydrogen sulfide (H 2 S) against ischemia/reperfusion injury in vivo: a systematic review and meta-analysis
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Pre- and postconditioning the heart with hydrogen sulfide (H 2 S) against ischemia/reperfusion injury in vivo: a systematic review and meta-analysis

机译:用硫化氢(H 2 S)预先处理心脏免受体内缺血/再灌注损伤的心脏:系统评价和荟萃分析

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摘要

Abstract Conditioning-like infarct limitation by enhanced level of hydrogen sulfide (H 2 S) has been demonstrated in many animal models of myocardial ischemia/reperfusion injury (MIRI) in vivo. We sought to evaluate the effect of H 2 S on myocardial infarction across in vivo pre-clinical studies of MIRI using a comprehensive systematic review followed by meta-analysis. Embase, Pubmed and Web of Science were searched for pre-clinical investigation of the effect of H 2 S on MIRI in vivo. Retained records (6031) were subjected to our pre-defined inclusion criteria then were objectively critiqued. Thirty-two reports were considered eligible to be included in this study and were grouped, based on the time of H 2 S application, into preconditioning and postconditioning groups. Data were pooled using random effect meta-analysis. We also investigated the possible impact of different experimental variables and the risk of bias on the observed effect size. Preconditioning with H 2 S ( n ?=?23) caused a significant infarct limitation of ??20.25% (95% CI ??25.02, ??15.47). Similarly, postconditioning with H 2 S ( n ?=?40) also limited infarct size by ??21.61% (95% CI ??24.17, ??19.05). This cardioprotection was also robust and consistent following sensitivity analyses where none of the pre-defined experimental variables had a significant effect on the observed infarct limitation. H 2 S shows a significant infarct limitation across in vivo pre-clinical studies of MIRI which include data from 825 animals. This infarct-sparing effect is robust and consistent when H 2 S is applied before ischemia or at reperfusion, independently on animal size or sulfide source. Validating this infarct limitation using large animals from standard medical therapy background and with co-morbidities should be the way forward.
机译:摘要在体内心肌缺血/再灌注损伤(MiRi)的许多动物模型中,证明了通过增强水平的硫化氢水平(H 2 S)的调理样梗塞限制。我们试图评估H 2 S对MIRI的体内临床研究中的心肌梗死的影响,使用综合系统评价,然后进行META分析。研讨,搜索了P 2 S对体内Miri效果的临床前调查。保留记录(6031)遭到我们预定义的纳入标准,然后客观批评。三十两份报告被认为有资格包含在本研究中,并根据H 2 S申请的时间分组,进入预处理和后处理组。使用随机效应元分析汇集数据。我们还调查了不同实验变量的可能影响以及对观察到的效果大小的偏置风险。用H 2 S(n?=Δ23)预处理导致梗死的显着梗塞限制20.25%(95%ci 25.02,?? 15.47)。类似地,与H 2 S(n?= 40)的后处理也有限的梗塞大小(21.61%(95%CI 24.17,?? 19.05)。这种心脏保护也是稳健的,并且在敏感性分析后,缺少预定义的实验变量没有关于观察到的梗塞限制的显着影响。 H 2 S显示了MIRI的体内临床研究中的显着梗塞限制,包括来自825只动物的数据。当在缺血之前施用H 2 S或在再灌注时,独立于动物尺寸或硫化物源时,这种梗死效果是稳健的并且一致。使用来自标准医疗疗法背景的大型动物验证这种梗塞限制,并与合作生命条件应该是前进的方向。

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