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Pre- and postconditioning the heart with hydrogen sulfide (H2S) against ischemia/reperfusion injury in vivo: a systematic review and meta-analysis

机译:用硫化氢(H2S)对心脏进行预处理和后处理以对抗体内缺血/再灌注损伤:系统评价和荟萃分析

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摘要

Conditioning-like infarct limitation by enhanced level of hydrogen sulfide (H2S) has been demonstrated in many animal models of myocardial ischemia/reperfusion injury (MIRI) in vivo. We sought to evaluate the effect of H2S 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 H2S 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 H2S 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 H2S (n = 23) caused a significant infarct limitation of − 20.25% (95% CI − 25.02, − 15.47). Similarly, postconditioning with H2S (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. H2S 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 H2S 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.Electronic supplementary materialThe online version of this article (10.1007/s00395-017-0664-8) contains supplementary material, which is available to authorized users.
机译:在体内心肌缺血/再灌注损伤(MIRI)的许多动物模型中均已证明,硫化氢(H2S)水平升高会引起类似条件的梗塞。我们试图通过综合的系统评价然后进行荟萃分析,评估MI2的体内临床前研究中H2S对心肌梗死的影响。搜寻Embase,Pubmed和Web of Science进行H2S对MIRI体内作用的临床前研究。保留记录(6031)符合我们预先定义的纳入标准,然后客观地进行了批评。 32份报告被认为符合纳入本研究的条件,并根据H2S的使用时间分为预处理和后处理组。使用随机效应荟萃分析汇总数据。我们还研究了不同实验变量的可能影响以及对观察到的效应大小产生偏见的风险。用H2S预处理(n = 23)导致的梗塞严重度限制为−20.25%(95%CI − 25.02,− 15.47)。同样,用H2S(n = 40)进行后处理也将梗死面积限制为-21.61%(95%CI-24.17,-19.05)。在进行敏感性分析后,这种心脏保护作用也很牢固且一致,在敏感性分析中,没有一个预定义的实验变量对观察到的梗死范围有显着影响。在MIRI的体内临床前研究中,H2S显示出明显的梗塞局限性,其中包括来自825只动物的数据。当在缺血前或再灌注时施用H2S时,无论动物大小或硫化物来源如何,均能有效地减少梗塞。使用标准药物治疗背景和合并症的大型动物来验证这种梗塞限制应该是前进的方向。电子补充材料本文的在线版本(10.1007 / s00395-017-0664-8)包含补充材料,可用于授权用户。

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