Department of Physiology [F.D., O.O., A.Z., V.T., M.H.], Department of Dermatology and Allergology [I.N.], Department of Medical Informatics [F.B.] University of Szeged School of Medicine, Szeged, H-6720, Hungary; Department of Pediatrics [P.T.], University Teaching Hospital Orosháza, Orosháza, H-5900, Hungary.

Abstract

Hydrogen (H2) has been reported to neutralize toxic reactive oxygen species (ROS). Oxidative stress is an important mechanism of neuronal damage after perinatal asphyxia. We examined if 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=8,7), and respective time control groups (n=9,7). Asphyxia was induced by suspending ventilation for 10 min, followed by reventilation with the respective gases for 4 hours. After euthanasia, the brains were processed for neuropathological examination. Pial arteriolar diameter changes to graded hypercapnia [5-10%CO2 inhalation] and NMDA, [10-4M]) were determined using the closed cranial window/intravital microscopy before and 1h 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 ROS-dependent CR to NMDA. In summary, H2-RA could be a promising approach to reduce the neurological deficits after perinatal asphyxia.

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