Argon reduces neurohistopathological damage and preserves functional recovery after cardiac arrest in rats

Brücken, Anne; Çizen, Ayşegül; Fera, Carmen; Meinhardt, Axel; Weis, Joachim; Nolte, Kay; Rossaint, Rolf; Pufe, Thomas; Marx, Gernot; Fries, Michael

doi:10.1093/bja/aes509

Cited by 64 publications

(69 citation statements)

References 41 publications

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“…A more pronounced beneficial effect regarding cell viability for postconditioning with argon was described vis-a-vis nitrogen and even xenon. Combining some features of the aforementioned models, some groups use a resuscitation model to induce cerebral ischemia: In pigs and rats postconditioning with 70% of argon resulted in improved neurological outcome [12,28]. The morphological extent of brain damage (at least for some regions) was reduced compared to controls.…”

Section: Discussionmentioning

confidence: 99%

Argon: Systematic Review on Neuro- and Organoprotective Properties of an “Inert” Gas

Höllig

Schug

Fahlenkamp

et al. 2014

IJMS

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Argon belongs to the group of noble gases, which are regarded as chemically inert. Astonishingly some of these gases exert biological properties and during the last decades more and more reports demonstrated neuroprotective and organoprotective effects. Recent studies predominately use in vivo or in vitro models for ischemic pathologies to investigate the effect of argon treatment. Promising data has been published concerning pathologies like cerebral ischemia, traumatic brain injury and hypoxic ischemic encephalopathy. However, models applied and administration of the therapeutic gas vary. Here we provide a systematic review to summarize the available data on argon’s neuro- and organoprotective effects and discuss its possible mechanism of action. We aim to provide a summary to allow further studies with a more homogeneous setting to investigate possible clinical applications of argon.

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Section: Discussionmentioning

confidence: 99%

Argon: Systematic Review on Neuro- and Organoprotective Properties of an “Inert” Gas

Höllig

Schug

Fahlenkamp

et al. 2014

IJMS

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show abstract

“…This proof-of-principle may also be extended to other interventions that appear promising based on single organ studies, such as cyclosporine postconditioning [25], inhalation of argon [18] or hydrogen [26].…”

Section: Discussionmentioning

confidence: 93%

“…The rat ventricular fibrillation/resuscitation model was based on several published rat resuscitation models from other research groups [15][16][17][18]. Buprenorphine (0.02 mg/kg) was administered subcutaneously as analgesic and pentobarbital (60 mg/kg) was administered intraperitonially for induction of anesthesia.…”

Section: Animal Preparationmentioning

confidence: 99%

Sildenafil Postconditioning in a Rat Model of Ventricular Fibrillation/ Resuscitation

Vanagt¹,

Amin²,

Brouwers³

et al. 2017

J Clin Exp Cardiolog

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Objective: To evaluate the multi-organ postconditioning potential of sildenafil during resuscitation. Circulatory arrest/resuscitation induces ischemia/reperfusion (I/R) injury in all organs. I/R injury can be reduced using postconditioning during reperfusion. Sildenafil has proven strong single-organ postconditioning properties.Methods: Ventricular fibrillation (VF) was induced and left untreated for 6 min in anesthetized adult male Wistar rats. During resuscitation, placebo (n=10) or intravenous sildenafil 0.2 mg/kg (n=10) was administered. Troponin-i release, lactate release, blood gases and hemodynamic parameters were assessed. After 3 h of reperfusion, rats were euthanized; brain and heart were removed for infarct staining with triphenyltetrazolium chloride. Urinary kidney injury molecule (KIM-1) was assessed. Data expressed as median (interquartile range), p<0.05 significant. Results:Resuscitation/defibrillation resulted in return of spontaneous circulation in all rats. Compared with the sildenafil group, the control group showed higher overall troponin release versus Sildenafil 16 (12-42) h·microg/L, p=0.032) and higher left ventricular infarct percentage versus Sildenafil 16 (12-18)%, p=0.039). There was no significant difference between the groups with respect to mortality, hemodynamic recovery, cerebral cortex infarct percentage, lactate release, blood gas values and urinary KIM-1 release. Three rats in the sildenafil group developed pulmonary edema versus none in the control group. Conclusions:Sildenafil postconditioning during resuscitation significantly reduces cardiac injury but does not affect mortality, cerebral and renal injury after resuscitation.

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“…The argon exposure protocols were defined empirically based on previous reports. Argon concentrations of 30-70% applied for 45-180 min had shown protective effects in previous studies [7,19]. The boxes were placed into an incubator and warmed to 37°C.…”

Section: Methodsmentioning

confidence: 99%

Argon Preconditioning Protects Airway Epithelial Cells against Hydrogen Peroxide-Induced Oxidative Stress

Hafner

Soto-Gonzalez

et al. 2016

Eur Surg Res

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Background: Oxidative stress is the predominant pathogenic mechanism of ischaemia-reperfusion (IR) injury. The noble gas argon has been shown to alleviate oxidative stress-related myocardial and cerebral injury. The risk of lung IR injury is increased in some major surgeries, reducing clinical outcome. However, no study has examined the lung-protective efficacy of argon preconditioning. The present study investigated the protective effects of argon preconditioning on airway epithelial cells exposed to hydrogen peroxide (H₂O₂) to induce oxidative stress. Methods: A549 airway epithelial cells were treated with a cytotoxic concentration of H₂O₂ after exposure to standard air or 30 or 50% argon/21% oxygen/5% carbon dioxide/rest nitrogen for 30, 45 or 180 min. Cells were stained with annexin V/propidium iodide, and apoptosis was evaluated by fluorescence-activated cell sorting. Protective signalling pathways activated by argon exposure were identified by Western blot analysis for phosphorylated candidate molecules of the mitogen-activated protein kinase and protein kinase B (Akt) pathways. Results: Preconditioning with 50% argon for 30, 45 and 180 min and 30% argon for 180 min caused significant protection of A549 cells against H₂O₂-induced apoptosis, with increases in cellular viability of 5-47% (p < 0.0001). A small adverse effect was also observed, which presented as a 12-15% increase in cellular necrosis in argon-treated groups. Argon exposure resulted in early activation of c-Jun N-terminal kinase (JNK) and p38, peaking 10- 30 min after the start of preconditioning, and delayed activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, peaking after 60-90 min. Conclusions: Argon preconditioning protects airway epithelial cells from H₂O₂-induced apoptotic cell death. Argon activates the JNK, p38, and ERK1/2 pathways, but not the Akt pathway. The cytoprotective properties of argon suggest possible prophylactic applications in surgery-related IR injury of the lungs.

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Argon reduces neurohistopathological damage and preserves functional recovery after cardiac arrest in rats

Abstract: Our study demonstrates that a single 1 h application of 70% argon significantly reduced histopathological damage of the neocortex and hippocampus, associated with a marked improvement in functional neurological recovery.

Cited by 64 publications

References 41 publications

Argon: Systematic Review on Neuro- and Organoprotective Properties of an “Inert” Gas

Argon: Systematic Review on Neuro- and Organoprotective Properties of an “Inert” Gas

Sildenafil Postconditioning in a Rat Model of Ventricular Fibrillation/ Resuscitation

Argon Preconditioning Protects Airway Epithelial Cells against Hydrogen Peroxide-Induced Oxidative Stress

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