Hydrogen is neuroprotective and preserves cerebrovascular reactivity in asphyxiated newborn pigs.
Hydrogen (H2) has been reported to neutralize toxic reactive oxygen species. Oxidative stress is an important mechanism of neuronal damage after perinatal asphyxia. We examined whether 2.1% H2-supplemented room air (H2-RA) ventilation would preserve cerebrovascular reactivity (CR) and brain morphology after asphyxia/reventilation (A/R) in newborn pigs. Anesthetized, ventilated piglets were assigned to one of the following groups: A/R with RA or H2-RA ventilation (A/R-RA and A/R-H2-RA; n = 8 and 7, respectively) and respective time control groups (n = 9 and 7). Asphyxia was induced by suspending ventilation for 10 min, followed by reventilation with the respective gases for 4 h. After euthanasia, the brains were processed for neuropathological examination. Pial arteriolar diameter changes to graded hypercapnia (5-10% CO2 inhalation), and NMDA (10(-4) M) were determined using the closed cranial window/intravital microscopy before and 1 h after asphyxia. Neuropathology revealed that H2-RA ventilation significantly reduced neuronal injury induced by A/R in virtually all examined brain regions including the cerebral cortex, the hippocampus, basal ganglia, cerebellum, and the brainstem. Furthermore, H2-RA ventilation significantly increased CR to hypercapnia after A/R (% vasodilation was 23 ± 4% versus 41 ± 9%, p < 0.05). H2-RA ventilation did not affect reactive oxygen species-dependent CR to NMDA. In summary, H2-RA could be a promising approach to reduce the neurologic deficits after perinatal asphyxia.
Domoki
Ferenc
F
Department of Physiology, University of Szeged School of Medicine, Szeged H-6720, Hungary. domoki@phys.szote.u-szeged.hu
Oláh
Orsolya
O
Zimmermann
Aliz
A
Németh
István
I
Tóth-Szuki
Valéria
V
Hugyecz
Marietta
M
Temesvári
Péter
P
Bari
Ferenc
F
D000818:Animals; D000831:Animals, Newborn; D001238:Asphyxia Neonatorum / Q000503:physiopathology*; D001774:Blood Chemical Analysis; D001921:Brain / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004195:Disease Models, Animal; D006439:Hemodynamics; D006801:Humans; D006859:Hydrogen / Q000494:pharmacology*; D006935:Hypercapnia / Q000378:metabolism; D007231:Infant, Newborn; D018696:Neuroprotective Agents / Q000494:pharmacology*; D013552:Swine
D018696:Neuroprotective Agents; D006859:Hydrogen