Helium preconditioning attenuates hypoxia/ischemia-induced injury in the developing brain

Liu, Yi; Xue, Feng; Liu, Guoke; Shi, Xiaoxuan; Liu, Yun; Liu, Wenwu; Luo, Xu; Sun, Xuejun; Kang, Zhiwei

doi:10.1016/j.brainres.2010.12.068

Cited by 27 publications

(27 citation statements)

References 31 publications

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“…The former is a transient phase owing to post-translational changes of preexisting proteins through signaling pathways [14,15], while the latter robust and long lasting phase develops over days and is mediated by protective gene expression and new protein synthesis [14]. Several studies aimed at elucidating effects of either pharmacological or mechanical preconditioning on outcomes of ischemia reperfusion (IR) injury [3,7,[16][17][18]. However, the complexity of the system confounds the outcomes.…”

Section: Introductionmentioning

confidence: 99%

“…However, the complexity of the system confounds the outcomes. Studies so far, have focused on the delayed stage following preconditioning episodes, but data on the early phase remains scarce [3,[16][17][18]. Accordingly, the current investigation aimed at defining the protective mechanisms involved in the efficacy of short repetitive ischemic episodes, IPC, in guarding against the subsequent deleterious effects of IR injury in the brain.…”

Section: Introductionmentioning

confidence: 99%

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Possible Involvement of Oxidative Stress and Inflammatory Mediators in the Protective Effects of the Early Preconditioning Window Against Transient Global Ischemia in Rats

et al. 2011

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Ischemic preconditioning (IPC), comprising exposure to sub-lethal short term ischemic events, has been shown to exert adaptive responses in many organs including the brain, thus guarding against exacerbations of ischemia reperfusion (IR). However, the mechanisms involved in the early phase of such a protection remain elusive; hence, the present study aimed to investigate the modulatory effect of preconditioning against IR induced injury on infarct size, free radicals, inflammatory/anti-inflammatory markers, caspase-3 and heat shock protein (HSP)70 in the rat hippocampus. To this end, male Wistar rats were divided into 3 groups, (1) sham operated (SO) control; (2) IPC, animals were subject to 3 episodes of ischemia (5 min) followed by reperfusion (10 min), afterwards rats underwent ischemia (15 min) followed by reperfusion (60 min); (3) IR animals were subjected to 15 min global ischemia followed by 60 min reperfusion. IR produced cerebral infarction accompanied by an imbalance in the hippocampal redox status, neutrophil infiltration, elevation in tumor necrosis factor (TNF)-α and prostaglandin (PG)E₂, besides reduction in interleukin (IL)-10 and nitric oxide (NO) levels. IPC reverted all changes except for PGE₂; however, neither HSP70 nor caspase-3 expression was altered following IR or IPC. The current study points thus towards the activation of the antioxidant system, anti-inflammatory pathway, as well as NO in the early phase of preconditioning protection.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Possible Involvement of Oxidative Stress and Inflammatory Mediators in the Protective Effects of the Early Preconditioning Window Against Transient Global Ischemia in Rats

et al. 2011

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“…The degree of protection was similar to preconditioning with isoflurane and IPC. Besides the cardioprotective effects of the noble gases, argon, helium, and xenon were shown to diminish neuronal injury after hypoxia or ischemia in different in vitro and in vivo models (13,14,22). Some studies elucidate the relevance of helium in in vivo experiments with conditions of early preconditioning, late preconditioning, and postconditioning (20,21).…”

Section: Discussionmentioning

confidence: 99%

“…Despite the fact that tissue oxygen is restored by reperfusion, the hepatocellular injury is aggravated by numerous mechanisms. Furthermore, xenon and helium reduce neuronal injury following hypoxic or ischemic brain injury (13,14). With onset of reperfusion, large amounts of reactive oxygen species are released, initiating cell damage (3), e.g., by lipid peroxidation (4).…”

Section: Introductionmentioning

confidence: 99%

Pretreatment With Helium Does Not Attenuate Liver Injury After Warm Ischemia-Reperfusion

Braun¹,

Plitzko

Bicknell

et al. 2014

Shock

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Preconditioning with noble gases serves as an effective strategy to diminish tissue injury in different organs. The aim of this study was to investigate the influence of pretreatment with the nonanesthetic noble gas helium on hepatic injury after warm ischemia and reperfusion (IR) in comparison to ischemic preconditioning (IPC). Anesthetized and ventilated rats were randomized into six groups (n = 8/group): sham: after laparotomy, the portal triad was exposed without clamping; IPC was performed with 10 min of partial liver ischemia and 10 min of reperfusion; HePC: three cycles of 5 min with inhalation of helium 70 vol% and intermittent washout; IR: 45 min of ischemia followed by 240 min of reperfusion; IPC-IR: IPC followed by hepatic IR; HePC-IR: pretreatment with helium 70 vol% followed by hepatic IR. Hepatic injury was evaluated by measurement of serum enzymes aspartate aminotransferase and alanine aminotransferase. Hepatic mRNA expression and serum levels of tumor necrosis factor α (TNF-α) and interleukin 10 (IL-10) were measured with real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Myeloperoxidase in liver tissue was assessed spectrophotometrically as a marker of neutrophil accumulation. mRNA levels of heme oxygenase 1 in liver tissue were assessed to investigate a protein of the most abundant protective system in the liver. Aspartate aminotransferase and alanine aminotransferase serum activities increased after hepatic IR (sham vs. IR; P < 0.05). The serum levels of liver enzymes after IR were significantly diminished with IPC (P < 0.05), whereas helium pretreatment had no effect. mRNA expression of TNF-α increased in all groups except IPC-IR compared with sham, whereas mRNA expression of IL-10 increased only after helium pretreatment. Serum levels of IL-10 were not affected by any intervention, whereas serum levels of TNF-α and liver myeloperoxidase were increased after IR, but not after HePC-IR. In conclusion, pretreatment with inhaled helium does not attenuate hepatic injury after warm IR of the liver, although there is evidence for a modulation of the inflammatory response.

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“…Exposure to heliox, in lieu of nitrogen-containing breathing gas, has been shown to have neuro-protective [1-3] and cardio-protective [4-7] effects in the setting of ischemia/ reperfusion. Suggested mechanisms for these beneficial effects include activation of mitochondrial Ca++ sensitive potassium channels [8], protective kinase-signaling cascades [7] and mild uncoupling leading to decreased ROS (reactive oxygen species) production [4].…”

Section: Introductionmentioning

confidence: 99%

Continuous Heliox Breathing and the Extent of Anatomic Zone of Noreflow and Necrosis Following Ischemia/Reperfusion in the Rabbit Heart

Hale¹,

VanDeripe²,

Kloner³

2014

TOCMJ

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Background:Nitrogen may contribute to reperfusion injury. Some studies have shown that helium as a replacement for nitrogen in breathing gas (heliox) reduces cell necrosis after ischemia/reperfusion when used in a preconditioning fashion (intermittent heliox exposure). Our aim was to test whether heliox, breathed continuously throughout the ischemic and reperfusion periods, reduced necrosis and a marker of reperfusion injury, the no-reflow phenomenon.Methods and Results:Anesthetized, open-chest rabbits received 30 min coronary artery occlusion/3 hrs reperfusion. Before CAO rabbits were randomized to heliox (30% oxygen + 70% helium, n=8) or air supplemented with oxygen to achieve blood gas values within physiologic range (n = 8). Rabbits received the appropriate mix during ischemic and reperfusion periods. Infarct size (% risk zone) and no-reflow defect were measured at the end of the reperfusion period. The ischemic risk zone was similar in both groups (28% of left ventricle in heliox and 29% in control). Heliox breathing did not reduce necrosis; infarct size, expressed as a percentage of the risk region was 44±4% in the heliox group and 49±5% in controls, p = 0.68. The extent of the no-reflow defect was not altered by heliox, either expressed as a percent of the risk region (29±4% in heliox and 28±3% in control) or as a percent of the necrotic zone (65±5% in heliox and 59±8% in control).Heliox treatment had no effect on hemodynamic parameters or arterial blood gas values.Conclusion:Continuous heliox breathing does not appear to be cardioprotective in the setting of acute myocardial infarction in the rabbit model. Heliox respiration administered during 30 minutes of ischemia and 180 minutes of reperfusion did not alter infarct size or the extent of no-reflow.

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Helium preconditioning attenuates hypoxia/ischemia-induced injury in the developing brain

Cited by 27 publications

References 31 publications

Possible Involvement of Oxidative Stress and Inflammatory Mediators in the Protective Effects of the Early Preconditioning Window Against Transient Global Ischemia in Rats

Possible Involvement of Oxidative Stress and Inflammatory Mediators in the Protective Effects of the Early Preconditioning Window Against Transient Global Ischemia in Rats

Pretreatment With Helium Does Not Attenuate Liver Injury After Warm Ischemia-Reperfusion

Continuous Heliox Breathing and the Extent of Anatomic Zone of Noreflow and Necrosis Following Ischemia/Reperfusion in the Rabbit Heart

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