Endogenous hydrogen sulfide contributes to the cardioprotective effects of pre-conditioning with endotoxin, but not ischaemia, in the rat

Sivarajah, Ahila; McDonald, Michelle C.; Thiemermann, C.; Harvey, William F.

doi:10.1016/j.yjmcc.2006.03.137

Cited by 1 publication

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Enhanced H 2 S level protects against myocardial infarction via preserving mitochondrial function [ 17 ], maintaining membrane integrity [ 17 , 65 ], limiting mitochondrial ROS generation [ 32 ] and inhibiting the opening of mitochondrial permeability transition pore (PTP) [ 10 , 32 , 65 ]. Moreover, mitochondrial K ATP channel is another target of H 2 S protection [ 54 , 55 , 57 ]. However, the question yet to be answered is how H 2 S triggers these signalling pathways to exert its infarct-limiting effect?…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it has been demonstrated that H 2 S activates PI3K/Akt signalling pathways through sulfhydrating phosphatase and tensin homolog (PTEN) abrogating its inhibitory effect [ 62 ]. Furthermore, sulfhydration is demonstrated to modify the activity of mitochondrial K ATP channel, another target of H 2 S [ 54 , 55 , 57 ], and ATP synthase (F 1 F 0 ATP synthase/complex V) [ 39 ], the current proposed main component of PTP, which either is known to protect the mitochondria and eventually limit infarct size. Taken together, the role of sulfhydration in conditioning with H 2 S needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

“…The search included the literature that investigated the effect of H 2 S on infarct size in in vivo models of MIRI, published between January 01, 2005 and December 16, 2016 considering that the first in vivo report was published in 2006 by Sivarajah et al [ 55 ]. The search only included studies which are available in English.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

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

2017

View full text Add to dashboard Cite

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.

show abstract