Argon Exposure Induces Postconditioning in Myocardial Ischemia–Reperfusion

Lemoine, Sandrine; Blanchart, Katrien; Souplis, Mathieu; Lemaître, Adrien; Legallois, Damien; Coulbault, Laurent; Simard, Christophe; Allouche, Stéphane; Abraini, Jacques H.; Hanouz, Jean‐Luc; Rouet, René; Sallé, Laurent; Guinamard, Romain; Manrique, Alain

doi:10.1177/1074248417702891

Cited by 28 publications

(38 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Its effect was found to be blunted by the pharmacological inhibition of phosphoinositide 3‐kinase or extracellular regulated kinase . The same findings were observed in an in vitro model of ischaemia–reperfusion in human atrial appendages . The protective effect of argon on functional recovery was, again, blunted by pharmacological inhibitors of phosphoinositide 3‐kinase, Akt and extracellular regulated kinase, and also by activators of mitochondrial permeability transition pore opening .…”

Section: Discussionsupporting

confidence: 64%

“…50%) might explain this absence of effect. Importantly, in addition to its well‐established neuroprotective effect, argon has also previously demonstrated nephroprotective and cardioprotective effects. In a rat model of myocardial ischaemia, argon administration after reperfusion prevented the decrease in left ventricular ejection fraction .…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, in addition to its well‐established neuroprotective effect, argon has also previously demonstrated nephroprotective and cardioprotective effects. In a rat model of myocardial ischaemia, argon administration after reperfusion prevented the decrease in left ventricular ejection fraction . A previous study also demonstrated a reduction in myocardial infarct size when argon was given as a preconditioning agent in a rabbit model of coronary obstruction .…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Argon attenuates multiorgan failure following experimental aortic cross‐clamping

Savary

Lidouren

Rambaud

et al. 2018

Brit J Clinical Pharma

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Argon attenuates multiorgan failure following experimental aortic cross‐clamping

Savary

Lidouren

Rambaud

et al. 2018

Brit J Clinical Pharma

View full text Add to dashboard Cite

show abstract

“…The protective effects of argon and xenon on cellular integrity have been shown for numerous conditions being at high risk for organ dysfunction or poor cerebral outcome, e.g. cardiac surgery 3–6 , cardiac resuscitation 7–10 , transplantation 11 or neurological disorders 12–18 . The mechanisms beyond xenon-induced neuroprotection comprise NMDA-antagonism and activation of two-pore potassium channels (TREK-1) or K ATP -channels 1 .…”

Section: Introductionmentioning

confidence: 99%

“…Referring the neuroprotective effects of argon, several mechanisms are discussed; e.g. activation of ERK1/2 and PI3K-AKT 3,19,20 , stimulation of TLR2/4 17,21,22 and up-regulation of the anti-apoptotic gene Bcl-2 18 . Recently, a common mechanism of argon and xenon has been identified.…”

Section: Introductionmentioning

confidence: 99%

Argon reduces the pulmonary vascular tone in rats and humans by GABA-receptor activation

Suleiman

Klassen

Katz

et al. 2019

Sci Rep

View full text Add to dashboard Cite

Argon exerts neuroprotection. Thus, it might improve patients’ neurological outcome after cerebral disorders or cardiopulmonary resuscitation. However, limited data are available concerning its effect on pulmonary vessel and airways. We used rat isolated perfused lungs (IPL) and precision-cut lung slices (PCLS) of rats and humans to assess this topic. IPL: Airway and perfusion parameters, oedema formation and the pulmonary capillary pressure (Pcap) were measured and the precapillary and postcapillary resistance (Rpost) was calculated. In IPLs and PCLS, the pulmonary vessel tone was enhanced with ET-1 or remained unchanged. IPLs were ventilated and PCLS were gassed with argon-mixture or room-air. IPL: Argon reduced the ET-1-induced increase of Pcap, Rpost and oedema formation (p < 0.05). PCLS (rat): Argon relaxed naïve pulmonary arteries (PAs) (p < 0.05). PCLS (rat/human): Argon attenuated the ET-1-induced contraction in PAs (p < 0.05). Inhibition of GABAB-receptors abolished argon-induced relaxation (p < 0.05) in naïve or ET-1-pre-contracted PAs; whereas inhibition of GABAA-receptors only affected ET-1-pre-contracted PAs (p < 0.01). GABAA/B-receptor agonists attenuated ET-1-induced contraction in PAs and baclofen (GABAB-agonist) even in pulmonary veins (p < 0.001). PLCS (rat): Argon did not affect the airways. Finally, argon decreases the pulmonary vessel tone by activation of GABA-receptors. Hence, argon might be applicable in patients with pulmonary hypertension and right ventricular failure.

show abstract

Gasotransmitters and noble gases in cardioprotection: unraveling molecular pathways for future therapeutic strategies

Pagliaro,

Weber,

Femminò

et al. 2024

Basic Res Cardiol

View full text Add to dashboard Cite

Despite recent progress, ischemic heart disease poses a persistent global challenge, driving significant morbidity and mortality. The pursuit of therapeutic solutions has led to the emergence of strategies such as ischemic preconditioning, postconditioning, and remote conditioning to shield the heart from myocardial ischemia/reperfusion injury (MIRI). These ischemic conditioning approaches, applied before, after, or at a distance from the affected organ, inspire future therapeutic strategies, including pharmacological conditioning. Gasotransmitters, comprising nitric oxide, hydrogen sulfide, sulfur dioxide, and carbon monoxide, play pivotal roles in physiological and pathological processes, exhibiting shared features such as smooth muscle relaxation, antiapoptotic effects, and anti-inflammatory properties. Despite potential risks at high concentrations, physiological levels of gasotransmitters induce vasorelaxation and promote cardioprotective effects. Noble gases, notably argon, helium, and xenon, exhibit organ-protective properties by reducing cell death, minimizing infarct size, and enhancing functional recovery in post-ischemic organs. The protective role of noble gases appears to hinge on their modulation of molecular pathways governing cell survival, leading to both pro- and antiapoptotic effects. Among noble gases, helium and xenon emerge as particularly promising in the field of cardioprotection. This overview synthesizes our current understanding of the roles played by gasotransmitters and noble gases in the context of MIRI and cardioprotection. In addition, we underscore potential future developments involving the utilization of noble gases and gasotransmitter donor molecules in advancing cardioprotective strategies.

show abstract

Argon Exposure Induces Postconditioning in Myocardial Ischemia–Reperfusion

Abstract: Argon has strong cardioprotective properties when applied in conditions of postconditioning and thus appears as a potential therapeutic tool in I/R situations.

Cited by 28 publications

References 51 publications

Argon attenuates multiorgan failure following experimental aortic cross‐clamping

Argon attenuates multiorgan failure following experimental aortic cross‐clamping

Argon reduces the pulmonary vascular tone in rats and humans by GABA-receptor activation

Gasotransmitters and noble gases in cardioprotection: unraveling molecular pathways for future therapeutic strategies

Contact Info

Product

Resources

About