Hydrogen is neuroprotective and preserves cerebrovascular reactivity in asphyxiated newborn pigs

Domoki, Ferenc; Oláh, Orsolya; Zimmermann, Aliz; Németh, István; Tóth‐Szűki, Valéria; Hugyecz, Marietta; Temesvári, Péter; Bari, Ferenc

doi:10.1203/pdr.0b013e3181f2e81c

Cited by 31 publications

(37 citation statements)

References 35 publications

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“…Experimental evidence from hypoxiaischaemia in pigs have shown a neuroprotective effect of topiramate, an anticonvulsant that may reduce excitotoxicity and calcium overload 208 , and of nicotine, which has antiapoptotic features and attenuates the post-hypoxic decrease in Brain-derived neurotrophic factor 209,210 . Finally, recent evidence from newborn pigs suggests a neuroprotective effect of reoxygenation with room-air supplemented with 2.1% hydrogen 211 .…”

Section: Combination With Pharmacological Agentsmentioning

confidence: 96%

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

et al. 2009

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Section: Combination With Pharmacological Agentsmentioning

confidence: 96%

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

et al. 2009

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“…In our study made on acute changes after birth asphyxia, asphyxia was shown to significantly increase the number of damaged neurons after 4 hours, moreover, hydrogen ventilation was shown to partially alleviate the hypoxic/ischemic neuronal damage [141]. However, we could not show statistically significant increases of COX-2 immunopositive neurons, perhaps there was a slight tendency for increased number of positive neurons after asphyxia in the parietal and occipital cortices.…”

Section: Map-2 Densitycontrasting

confidence: 66%

“…Indeed, the magnitude of pial arteriolar diameter changes in response to these stimuli was virtually identical to those determined in the acute model of brain asphyxia [65,69,141].…”

Section: Map-2 Densitysupporting

confidence: 65%

“…We also showed the protective effect of H 2 on CR in the early and the delayed reventilation period. The whole range of the biological effects of H 2 is not yet of H 2 plausibly explained the observed protection [141], because the mechanism of CR impairment involves ROS. In the delayed birth asphyxia model H 2 ventilation was given for 4 hours starting immediately after the asphyxia and thus stopped 20 hours before the CR measurements excluding the possibility of the direct involvement of H 2 on the observed preservation to CR.…”

Section: Map-2 Densitymentioning

confidence: 97%

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Hydrogen is neuroprotective and preserves neurovascular reactivity following asphyxia in newborn pigs

Oláh¹

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“…Accordingly, various antioxidant approaches have been shown to prevent the acute attenuation of CR in the piglet. Recently, molecular hydrogen (H 2 ) - a putative selective inhibitor of hydroxyl radicals [11] - was found to prevent acute post-asphyxic CR impairment with a concomitant neuroprotective effect in piglets [12]. …”

Section: Introductionmentioning

confidence: 99%

Delayed Neurovascular Dysfunction Is Alleviated by Hydrogen in Asphyxiated Newborn Pigs

Oláh¹,

Tóth‐Szűki²,

Temesvári

et al. 2013

Neonatology

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Background: The neurovascular unit encompasses the functional interactions of cerebrovascular and brain parenchymal cells necessary for the metabolic homeostasis of neurons. Previous studies indicated marked but only transient (1-4 h) reactive oxygen species-dependent neurovascular dysfunction in newborn pigs after severe hypoxic/ischemic (H/I) stress contributing to the neuronal injury after birth asphyxia. Objectives: Our major purpose was to determine if neurovascular dysfunction would also occur later, at 24 h after a milder H/I stress. We also tested if the putative hydroxyl radical scavenger hydrogen (H₂) exerted neurovascular protection. Methods: Anesthetized, ventilated piglets were assigned to three groups of 9 animals: time control, asphyxia/reventilation with air, and asphyxia/reventilation with air +2.1% H₂ for 4 h. Asphyxia was induced by suspending ventilation for 8 min. Cerebrovascular reactivity (CR) of pial arterioles was determined using closed cranial window/intravital microscopy 24 h after asphyxia to the endothelium-dependent cerebrovascular stimulus hypercapnia, the neuronal function-dependent stimulus N-methyl-D-aspartate (NMDA), norepinephrine, and sodium nitroprusside. The brains were subjected to histopathology. Results: Hemodynamic parameters, blood gases, and core temperature did not differ significantly among the experimental groups. In the early reventilation period, the recovery of electroencephalographic activity was significantly better in H₂-treated animals. Asphyxia/reventilation severely attenuated CR to hypercapnia and NMDA; however, reactivity to norepinephrine and sodium nitroprusside were unaltered. H₂ fully or partially preserved CR to hypercapnia or NMDA, respectively. Histopathology revealed modest neuroprotection afforded by H₂. Conclusions: Severe stimulus-selective delayed neurovascular dysfunction develops and persists even after mild H/I stress. H₂ alleviates this delayed neurovascular dysfunction that can contribute to its neuroprotective effect.

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Hydrogen is neuroprotective and preserves cerebrovascular reactivity in asphyxiated newborn pigs

Abstract: Hydrogen (H 2

Cited by 31 publications

References 35 publications

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

Hydrogen is neuroprotective and preserves neurovascular reactivity following asphyxia in newborn pigs

Delayed Neurovascular Dysfunction Is Alleviated by Hydrogen in Asphyxiated Newborn Pigs

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