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

Abstract

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.

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

“…This point has been further validated by later studies that confirm mtROS production mainly takes place at the electron transport chain localized on the inner mitochondrial membrane during the process of oxidative phosphorylation [57,58]. Mechanistically, the primary sites of superoxide anion production and release are Complex I (NADH-ubiquinone oxidoreductase), Complex II (succinate dehydrogenase, SDH), and Complex III (ubiquinol-cyctochrome c oxidoreductase) [59]. Complexes I and II accept electrons from NADH + H + and FADH 2 , respectively, which are transferred to Complex III and finally to Complex IV (cytochrome c oxidase), where the final electron acceptor is oxygen and the final product is water [60].…”

Suppression of Tafazzin promotes thyroid cancer apoptosis via activating the JNK signaling pathway and enhancing INF2‐mediated mitochondrial fission

“…TUNEL staining was performed using a One Step TUNEL Apoptosis Assay Kit (Cat. No: C1086; Beyotime) according to the manufacturer's instructions (Karwi, Bice, & Baxter, ). The 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay was performed according to the methods used in a previous study (Kelly et al, ).…”

Diabetic keto acidosis as a deceiving presentation to simultaneous aortic and tricuspid infective endocarditis

“…Within the vascular wall, several pathways produce H 2 S. A recent study by Leskova and co-workers in cultured HUVECS observed that these cells take up exogenous thiosulfate for later release as free H 2 S while numerous other studies report H 2 S production in the vascular wall by cystathionine gamma-lyase (CSE) [1][2][3][4][5][6][7], cystathionine betasynthase (CBS) [8][9][10] and 3-mercaptopyruvate sulfurtransfurase (3-MST) [11,12]. Thus, the synthesis of this gasotransmitter is not completely defined and remains an area of active investigation as discussed below.…”

“…Hydrogen sulfide (H2S) acts on the vasculature throughout the body to elicit protective and beneficial actions. In addition, it has direct effects on cardiac muscle [1] and on renal tissues [22] demonstrating the ability of H 2 S to stabilize and enhance activity of eNOS. Taken together, H 2 S increases eNOS expression, stability, and activation, ultimately leading to elevate NO production.…”