Hydrogen sulfide reduces regional myocardial ischemia injury through protection of mitochondrial function

Xie, Yinghua; Zhang, Nan; Li, Lanfang; Qin-zeng, Zhang; Xie, Lijun; Jiang, Hong; Li, Liping; Hao, Na; Zhang, Jianxin

doi:10.3892/mmr.2014.2391

Cited by 18 publications

(13 citation statements)

References 54 publications

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“…In addition, the role of K ATP channels in mediating responses to H 2 S may depend on species and the vascular the preparation studied. Although Na 2 S and NaHS have a short duration of action, these H 2 S donors have been used as pharmacologic agents in the treatment of cardiac I/R injury (13,32,45). The mechanism of the putative vascular effect of the H 2 S donors promoting vasodilation is not clarified in the present study and needs more direct examination in better controlled experiments.…”

Section: Discussionmentioning

confidence: 79%

Analysis of cardiovascular responses to the H₂S donors Na₂S and NaHS in the rat

Yoo

Jupiter

Pankey

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Hydrogen sulfide (H2S) is an endogenous gaseous molecule formed from L-cysteine in vascular tissue. In the present study, cardiovascular responses to the H2S donors Na2S and NaHS were investigated in the anesthetized rat. The intravenous injections of Na2S and NaHS 0.03-0.5 mg/kg produced dose-related decreases in systemic arterial pressure and heart rate, and at higher doses decreases in cardiac output, pulmonary arterial pressure, and systemic vascular resistance. H2S infusion studies show that decreases in systemic arterial pressure, heart rate, cardiac output, and systemic vascular resistance are well-maintained, and responses to Na2S are reversible. Decreases in heart rate were not blocked by atropine, suggesting that the bradycardia was independent of parasympathetic activation and was mediated by an effect on the sinus node. The decreases in systemic arterial pressure were not attenuated by hexamethonium, glybenclamide, N(w)-nitro-L-arginine methyl ester hydrochloride, sodium meclofenamate, ODQ, miconazole, 5-hydroxydecanoate, or tetraethylammonium, suggesting that ATP-sensitive potassium channels, nitric oxide, arachidonic acid metabolites, cyclic GMP, p450 epoxygenase metabolites, or large conductance calcium-activated potassium channels are not involved in mediating hypotensive responses to the H2S donors in the rat and that responses are not centrally mediated. The present data indicate that decreases in systemic arterial pressure in response to the H2S donors can be mediated by decreases in vascular resistance and cardiac output and that the donors have an effect on the sinus node independent of the parasympathetic system. The present data indicate that the mechanism of the peripherally mediated hypotensive response to the H2S donors is uncertain in the intact rat.

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Section: Discussionmentioning

confidence: 79%

Analysis of cardiovascular responses to the H₂S donors Na₂S and NaHS in the rat

Yoo

Jupiter

Pankey

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…A considerable number of studies have been performed to examine the cardioprotective effects of H 2 S and NO, and the interactions between them in I/R injury, by employing several in vitro and in vivo experimental models of cardiac injury, including cultured cardiomyocytes, isolated perfused hearts, and rodent and large animal (rabbit, dog, pig) models (17,(22)(23)(24)(25)(26). However, to the best of our knowledge, no study has examined the effect of NaHS, PAG and L-NAME on isolated rat heart administered, and the present study is the first to establish the role of these donors and inhibitors in cardioprotection against I/R injury in rat heart.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart

Üstünova

Takır

Yilmazer

et al. 2020

In Vivo

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Background/Aim: This study was designed to provide further evidence for the interactions between hydrogen sulfide (H 2 S) and nitric oxide (NO) in ischemia/reperfusion (I/R) injury. Materials and Methods: Rat hearts were studied with the Langendorff technique using the H 2 S donor sodium hydrosulfide (NaHS, 40 μM) and the cystathionine gamma-lyase (CTH or CSE) inhibitor DLpropargylglycine (PAG, 1 mM). NO synthase inhibitor L-NGnitroarginine methyl ester (L-NAME, 30 mg/kg, 7 days) was administered before the isolation. The hearts were homogenized for biochemical and molecular analysis. Results: NaHS reversed I/R-induced cardiac performance impairment, increased tissue nitric oxide production and decreased tissue markers for cardiac injury, while L-NAME inhibited these effects. The expression of CTH was increased with PAG, which was suppressed by L-NAME. Conclusion: H 2 S and NO increase each other's production suggesting their interaction and cooperation in cardioprotection against I/R injury. Nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H 2 S), in the order of their discovery, are gasotransmitters, a term that refers to a gaseous transmitter, and was first coined by Wang (1). All are endogenously produced small signaling molecules with low molecular weight (NO, 30 Da; CO, 28 Da; H 2 S, 34 Da). Because they are small gaseous molecules, they reach easily their intracellular targets to activate them, by diffusing freely across the plasma membrane. They play a pivotal roles in the control of many physiological functions, including regulation of cardiovascular, nervous, gastrointestinal, excretory, immune, and reproductive systems (2-5). Of these three gaseous transmitters, H 2 S that was first introduced as a metabolic product in mammals by the American biochemist Vincent Du Vigneaud, has gained much attention in recent years due to its involvement in the above-mentioned physiological functions (2, 6, 7). It is endogenously synthesized in most mammalian tissues from L-cysteine and/or L-homocysteine by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CTH or CSE), and cysteine aminotransferase together with 3-mercaptopyruvate sulfurtransferase (2, 4, 8). Heart failure, the major health issue in the world and the leading cause of deaths, is a complicated disease caused by 2507 This article is freely accessible online.

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“…Hydrogen sulfide gas has recently been proposed as a potent gasotransmitter that may be responsible for the protection of ischemic tissues (17,(27)(28)(29). H 2 S has been observed to act like a free radical scavenger, to protect against cellular apoptosis, and to promote vasodilation (30).…”

Section: Discussionmentioning

confidence: 99%

Stem Cell Therapy and Hydrogen Sulfide: Conventional or Nonconventional Mechanisms of Action?

Jensen

Drucker

Olson

et al. 2019

Shock

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Purpose: Hydrogen sulfide (H 2 S) has many beneficial biological properties, including the ability to promote vasodilation. It has been shown to be released from stem cells and increased by hypoxia. Therefore, H 2 S may be an important paracrine factor in stem cell mediated intestinal protection. We hypothesized that hydrogen sulfide created through conventional pathways would be a critical component of stem cell mediated intestinal protection following ischemic injury.Methods: Human bone marrow derived mesenchymal stem cells (BMSCs) were transfected with negative control siRNA (Scramble), or with siRNA to CBS, MPST, or CTH.Knockdown was confirmed with PCR and hydrogen sulfide gas assessed with AzMC fluorophore. Eight week old male mice then underwent intestinal ischemia for 60 mins, after which time, perfusion was restored. BMSCs from each of the above groups were then placed into the mouse abdominal cavity prior to final closure. After 24 hours, mice were reanesthetized and mesenteric perfusion was assessed by Laser Doppler Imaging (LDI).Animals were then sacrificed and intestines excised, placed in formalin, paraffin embedded, and stained with H & E. Intestines were then scored with a common mucosal injury grading scale.Results: PCR confirmed knockdown of conventional H 2 S producing enzymes (CBS, MPST, CTH). Hydrogen sulfide gas was decreased in MPST and CTH transfected cells in normoxic conditions but was not decreased compared to scramble in any of the transfected groups in hypoxic conditions. BMSCs promoted increased mesenteric perfusion at 24 hours postischemia compared to vehicle. Transfected stem cells provided equivalent protection.Histologic injury was improved with BMSCs compared to vehicle. CBS, MPST, and CTH knockdown cell lines did not have any worse histological injury compared to Scramble.

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Hydrogen sulfide reduces regional myocardial ischemia injury through protection of mitochondrial function

Cited by 18 publications

References 54 publications

Analysis of cardiovascular responses to the H₂S donors Na₂S and NaHS in the rat

Analysis of cardiovascular responses to the H₂S donors Na₂S and NaHS in the rat

Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart

Stem Cell Therapy and Hydrogen Sulfide: Conventional or Nonconventional Mechanisms of Action?

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Hydrogen sulfide reduces regional myocardial ischemia injury through protection of mitochondrial function

Cited by 18 publications

References 54 publications

Analysis of cardiovascular responses to the H2S donors Na2S and NaHS in the rat

Analysis of cardiovascular responses to the H2S donors Na2S and NaHS in the rat

Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart

Stem Cell Therapy and Hydrogen Sulfide: Conventional or Nonconventional Mechanisms of Action?

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Analysis of cardiovascular responses to the H₂S donors Na₂S and NaHS in the rat

Analysis of cardiovascular responses to the H₂S donors Na₂S and NaHS in the rat