TY - CHAP
T1 - Protective effect of hydrogen gas therapy after germinal matrix hemorrhage in neonatal rats
AU - Lekic, Tim
AU - Manaenko, Anatol
AU - Rolland, William
AU - Fathali, Nancy
AU - Peterson, Mathew
AU - Tang, Jiping
AU - Zhang, John H.
N1 - Funding Information:
Acknowledgements This study was partially supported by a grant (NS053407) from the National Institutes of Health to J.H.Z. Conflict of interest statement
PY - 2011/1/1
Y1 - 2011/1/1
N2 - Background: Germinal matrix hemorrhage (GMH) is a neurological disease of very low birth weight premature infants leading to post-hemorrhagic hydrocephalus, cerebral palsy, and mental retardation. Hydrogen (H2) is a potent antioxidant shown to selectively reverse cytotoxic oxygen-radical injury in the brain. This study investigated the therapeutic effect of hydrogen gas after neonatal GMH injury. Methods: Neonatal rats underwent stereotaxic infusion of clostridial collagenase into the right germinal matrix brain region. Cognitive function was assessed at 3 weeks, and then sensorimotor function, cerebral, cardiac and splenic growths were measured 1 week thereafter. Results: Hydrogen gas inhalation markedly suppressed mental retardation and cerebral palsy outcomes in rats at the juvenile developmental stage. The administration of H2 gas, early after neonatal GMH, also normalized the brain atrophy, splenomegaly and cardiac hypertrophy 1 month after injury. Conclusion: This study supports the role of cytotoxic oxygen-radical injury in early neonatal GMH. Hydrogen gas inhalation is an effective strategy to help protect the infant brain from the post-hemorrhagic consequences of brain atrophy, mental retardation and cerebral palsy. Further studies are necessary to determine the mechanistic basis of these protective effects. © 2011 Springer-Verlag/Wien.
AB - Background: Germinal matrix hemorrhage (GMH) is a neurological disease of very low birth weight premature infants leading to post-hemorrhagic hydrocephalus, cerebral palsy, and mental retardation. Hydrogen (H2) is a potent antioxidant shown to selectively reverse cytotoxic oxygen-radical injury in the brain. This study investigated the therapeutic effect of hydrogen gas after neonatal GMH injury. Methods: Neonatal rats underwent stereotaxic infusion of clostridial collagenase into the right germinal matrix brain region. Cognitive function was assessed at 3 weeks, and then sensorimotor function, cerebral, cardiac and splenic growths were measured 1 week thereafter. Results: Hydrogen gas inhalation markedly suppressed mental retardation and cerebral palsy outcomes in rats at the juvenile developmental stage. The administration of H2 gas, early after neonatal GMH, also normalized the brain atrophy, splenomegaly and cardiac hypertrophy 1 month after injury. Conclusion: This study supports the role of cytotoxic oxygen-radical injury in early neonatal GMH. Hydrogen gas inhalation is an effective strategy to help protect the infant brain from the post-hemorrhagic consequences of brain atrophy, mental retardation and cerebral palsy. Further studies are necessary to determine the mechanistic basis of these protective effects. © 2011 Springer-Verlag/Wien.
KW - Hydrogen gas
KW - Neurological deficits
KW - Stroke, experimental
KW - Animals, Newborn
KW - Neuroprotective Agents/administration & dosage
KW - Cerebral Hemorrhage/chemically induced
KW - Psychomotor Performance/drug effects
KW - Functional Laterality/drug effects
KW - Rats
KW - Hydrogen/administration & dosage
KW - Gases/administration & dosage
KW - Posture
KW - Cognition Disorders/drug therapy
KW - Nervous System Diseases/drug therapy
KW - Animals
KW - Analysis of Variance
KW - Collagenases/toxicity
KW - Reaction Time/drug effects
KW - Somatosensory Disorders/drug therapy
KW - Organ Size/drug effects
KW - Disease Models, Animal
KW - Reflex/drug effects
UR - https://www.scopus.com/pages/publications/79960677177
UR - https://www.scopus.com/pages/publications/79960677177#tab=citedBy
UR - https://www.mendeley.com/catalogue/fd463f5b-2842-3617-8d02-11ca9274a5a9/
U2 - 10.1007/978-3-7091-0693-8_40
DO - 10.1007/978-3-7091-0693-8_40
M3 - Chapter
C2 - 21725762
SN - 9783709106921
SN - 978-3-7091-2007-1
T3 - Acta Neurochirurgica, Supplementum
SP - 237
EP - 241
BT - Intracerebral Hemorrhage Research
PB - Springer Vienna
ER -