Cellular Effects of Helium in Different Organs

Department of Anesthesiology, Laboratory of Experimental Intensive Care and Anesthesiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Anesthesiology (Impact Factor: 6.17). 06/2010; 112(6):1503-10. DOI: 10.1097/ALN.0b013e3181d9cb5e
Source: PubMed

ABSTRACT Experimental research in cardiac and neuronal tissue has shown that besides volatile anesthetics and xenon, the nonanesthetic noble gas helium also reduces ischemia-reperfusion damage. Even though the distinct mechanisms of helium-induced organ protection are not completely unraveled, several signaling pathways have been identified. Beside the protective effects on heart and brain that are mainly obtained by different pre- and postconditioning protocols, helium also exerts effects in the lungs, the immune system, and the blood vessels. Obviously, this noble gas is biochemically not inert and exerts biologic effects, although until today the question remains open on how these changes are mediated. Because of its favorable characteristics and the lack of hemodynamic side effects, helium is suitable for use also in critically ill patients. This review covers the cellular effects of helium, which may lead to new clinical strategies of tissue salvage in ischemia-reperfusion situations, both within and outside the perioperative setting.

1 Follower
  • [Show abstract] [Hide abstract]
    ABSTRACT: Helium, a noble gas, has been safely used in humans. In animal models of regional myocardial ischemia/reperfusion it was shown that helium conditioning reduces infarct size. Currently it is not known how helium exerts its cytoprotective effects and which cell death/survival pathways are affected. The objective of this study was therefore to investigate the cell protective effects of helium postconditioning by PCR array analysis of genes involved in necrosis, apoptosis, and autophagy. Male rats were subjected to 25 min of ischemia and 5, 15, or 30 min of reperfusion. Semiquantitative histological analysis revealed that 15 min of helium postconditioning reduced the extent of ischemia/reperfusion-induced cell damage. This effect was not observed after 5 and 30 min of helium postconditioning. Analysis of the differential expression of genes showed that 15 min of helium postconditioning mainly caused upregulation of genes involved in autophagy and inhibition of apoptosis versus ischemia/reperfusion alone. The results suggest that the cytoprotective effects of helium inhalation may be caused by a switch from pro-cell death signaling to activation of cell survival mechanisms, which appears to affect a wide range of pathways.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Postconditioning of myocardial tissue employs short cycles of ischemia or pharmacologic agents during early reperfusion. Effects of helium postconditioning protocols on infarct size and the ischemia/reperfusion-induced immune response were investigated by measurement of protein and mRNA levels of proinflammatory cytokines. Rats were anesthetized with S-ketamine (150 mg/kg) and diazepam (1.5 mg/kg). Regional myocardial ischemia/reperfusion was induced; additional groups inhaled 15, 30, or 60 min of 70% helium during reperfusion. Fifteen minutes of helium reduced infarct size from 43% in control to 21%, whereas 30 and 60 minutes of helium inhalation led to an infarct size of 47% and 39%, respectively. Increased protein levels of cytokine-induced neutrophil chemoattractant (CINC-3) and interleukin-1 beta (IL-1β) were found after 30 or 60 min of helium inhalation, in comparison to control. 30 min of helium increased mRNA levels of CINC-3, IL-1β, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) in myocardial tissue not directly subjected to ischemia/reperfusion. These results suggest that the effectiveness of the helium postconditioning protocol is very sensitive to duration of noble gas application. Additionally, helium was associated with higher levels of inflammatory cytokines; however, it is not clear whether this is causative of nature or part of an epiphenomenon.
    Journal of Immunology Research 01/2015; 2015:216798. DOI:10.1155/2015/216798 · 2.93 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: In neonatal respiratory distress syndrome (RDS) and acute RDS (ARDS) mechanical ventilation is often necessary to manage hypoxia, whilst protecting the lungs through lower volume ventilation and permissive hypercapnia. Mechanical ventilation can, however, induce or aggravate the lung injury caused by the respiratory distress. Helium, in a gas mixture with oxygen (heliox), has a low density and can reduce the flow in narrow airways and allow for lower driving pressures. Objectives: The aim of this study was to review preclinical and clinical studies of the use of heliox ventilation in acute lung injury associated with respiratory failure. Methods: A systematic search was executed in the PubMed and EMBASE databases, with search terms referring to ARDS or an acute lung injury condition associated with respiratory failure and the corresponding intervention. Results: A total of 576 papers were retrieved. After the majority had been excluded 20 papers remained, of which 6 articles described animal models (3 paediatric; 3 adult animal models) and 14 were clinical studies, of which 12 described paediatric patient populations and 2 adult patient populations. In both paediatric and adult animal models, heliox improved gas exchange while allowing for less invasive ventilation in a wide variety of models using different ventilation modes. Clinical studies show a reduction in the work of breathing during heliox ventilation, with a concomitant increase in pH and decrease in PaCO2 levels compared to oxygen ventilation. Conclusions: Although evidence so far is limited, there may be a rationale for heliox ventilation in ARDS as an intervention to improve ventilation and reduce the work of breathing. © 2015 S. Karger AG, Basel.