Oxidative stress, brain white matter damage andintrauterine asphyxia in fetal lambs

Ikeda, Tomoaki; Choi, BongKyoo; Yee, Simon; Murata, Yuji; Quilligan, Edward J.

doi:10.1016/s0736-5748(98)00055-0

Cited by 45 publications

(34 citation statements)

References 43 publications

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“…In fact, a more variable degree of white matter injury was detected in near-term sheep after several insults (Clapp et al, 1988;Penning et al, 1994;Mallard et al, 1998;Ikeda et al, 1999;Ohyu et al, 1999;Raad et al, 1999). Future studies are needed to determine whether acceleration of OL differentiation might be a feasible strategy to reduce the incidence and severity of PWMI.…”

Section: Discussionmentioning

confidence: 99%

Spatial Heterogeneity in Oligodendrocyte Lineage Maturation and Not Cerebral Blood Flow Predicts Fetal Ovine Periventricular White Matter Injury

Riddle¹,

Luo²,

Manese³

et al. 2006

J. Neurosci.

167

223

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Although periventricular white matter injury (PWMI) is the leading cause of chronic neurological disability and cerebral palsy in survivors of premature birth, the cellular-molecular mechanisms by which ischemia-reperfusion contributes to the pathogenesis of PWMI are not well defined. To define pathophysiologic relationships among ischemia, acute cerebral white matter damage, and vulnerable target populations, we used a global cerebral ischemia-reperfusion model in the instrumented 0.65 gestation fetal sheep. We developed a novel method to make repeated measurements of cerebral blood flow using fluorescently labeled microspheres to resolve the spatial heterogeneity of flow in situ in three-dimensional space. Basal flow in the periventricular white matter (PVWM) was significantly lower than in the cerebral cortex. During global cerebral ischemia induced by carotid occlusion, flow to all regions was reduced by nearly 90%. Ischemia of 30 or 37 min duration generated selective graded injury to frontal and parietal PVWM, two regions of predilection for human PWMI. Injury was proportional to the duration of ischemia and increased markedly with 45 min of ischemia to extensively damage cortical and subcortical gray matter. Surprisingly, the distribution of PVWM damage was not uniform and not explained by heterogeneity in the degree of white matter ischemia. Rather, the extent of white matter damage coincided with the presence of a susceptible population of late oligodendrocyte progenitors. These data support that although ischemia is necessary to generate PWMI, the presence of susceptible populations of oligodendrocyte progenitors underlies regional predilection to injury.

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Section: Discussionmentioning

confidence: 99%

Spatial Heterogeneity in Oligodendrocyte Lineage Maturation and Not Cerebral Blood Flow Predicts Fetal Ovine Periventricular White Matter Injury

Riddle¹,

Luo²,

Manese³

et al. 2006

J. Neurosci.

167

223

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“…Modified from Riddle et al 30 detected in near-term sheep after several insults. 35,37,38,[57][58][59] Hence, it appears that targeted death of preOLs could contribute to the pathogenesis of PWMI across a broad range of gestational ages and in multiple susceptible regions.…”

Section: Back Et Al Vulnerability Of Perinatal White Matter 727mentioning

confidence: 99%

Maturation-Dependent Vulnerability of Perinatal White Matter in Premature Birth

Back

Riddle

McClure

2007

Stroke

316

257

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Abstract-Survivors of premature birth have a predilection for perinatal brain injury, especially to periventricular cerebral white matter. Periventricular white matter injury (PWMI) is now the most common cause of brain injury in preterm infants and the leading cause of chronic neurological morbidity. The spectrum of chronic PWMI includes focal cystic necrotic lesions (periventricular leukomalacia) and diffuse myelination disturbances. Recent neuroimaging studies support that the incidence of periventricular leukomalacia is declining, whereas focal or diffuse noncystic injury is emerging as the predominant lesion. In a significant number of infants, PWMI appears to be initiated by perturbations in cerebral blood flow that reflect anatomic and physiological immaturity of the vasculature. Ischemic cerebral white matter is susceptible to pronounced free radical-mediated injury that particularly targets immature stages of the oligodendrocyte lineage. Emerging experimental data supports that pronounced ischemia in the periventricular white matter is necessary but not sufficient to generate the initial injury that leads to PWMI. The developmental predilection for PWMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible oligodendrocyte progenitors. Injury to oligodendrocyte progenitors may contribute to the pathogenesis of PWMI by disrupting the maturation of myelin-forming oligodendrocytes. There has been substantial recent progress in the understanding of the cellular and molecular pathogenesis of PWMI. The oligodendrocyte progenitor is a key target for preventive strategies to reduce ischemic cerebral white matter injury in premature infants. Key Words: hypoxia-ischemia Ⅲ oligodendrocyte Ⅲ prematurity P eriventricular white matter injury (PWMI) is the major form of brain injury and the leading cause of chronic neurological disability in survivors of premature birth. 1,2 Although major advances in the care of premature infants have resulted in striking improvements in the survival of very-low birth weight infants (Ͻ1.5 kg), when compared with the 1980s, improved survival has been accompanied by a significant increase in the number of preterm survivors with long-term neurological deficits. 3 In up to 25% of preterm survivors, the major consequence of PWMI is permanent motor impairment (ie, "cerebral palsy") ranging from mild to profound spastic motor deficits. 4,5 By school age, 25% to 50% of children with PWMI manifest a broad spectrum of cognitive and learning disabilities. 6 The period of highest risk for PWMI is between approximately 23 and 32 weeks postconceptional age. Premature infants with PWMI are at markedly increased risk for several others forms of brain injury, notably intraventricular hemorrhage and intraparenchymal hemorrhage. 1 Whereas medical interventions have resulted in a pronounced decrease in the incidence of intraventricular hemorrhage, 7,8 the incidence of PWMI is not decreasing. 9 Thus, PWMI is now the major neurological p...

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“…Ikeda et al [108] examined the role of oxidative stress in asphyxia-induced perinatal brain damage in near-term fetal lambs subjected to umbilical cord occlusion for approximately 60 min until fetal arterial pH diminished to less than 6.9 and base excess to less than -20 mEq/l. The results suggest that the developing telencephalic white matter is the most susceptible to the effects of intrauterine fetal asphyxia and that oxidative stress may be a major contributing factor to the pathogenesis of perinatal hypoxic-ischemic encephalopathy.…”

Section: Oxidative Stress and Perinatal Asphyxiamentioning

confidence: 99%

Causes of Oxidative Stress in the Pre- and Perinatal Period

et al. 2002

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Oxidative stress may be defined as an imbalance between pro-oxidant and antioxidant forces resulting in an overall pro-oxidant insult. Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, augmented levels of oxidative stress would be expected. Arguments for a role of oxidative stress/oxidative lipid derivatives in the pathogenesis of preeclampsia are documented in many papers and evidence continues to accumulate that oxidative stress is a mediator of endothelial dysfunction and thus contributes to the cardiovascular complications of preeclampsia. Also other conditions, such as toxic substance exposure, smoking and asphyxia likewise induce oxidative stress. The oxidized lipid products generated as a consequence of these conditions are highly reactive and cause damage to cells and cell membranes. Thus, increased oxidative stress accompanied by reduced endogenous defences may play a role in the pathogenesis of a number of diseases in the newborn.

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Oxidative stress, brain white matter damage andintrauterine asphyxia in fetal lambs

Cited by 45 publications

References 43 publications

Spatial Heterogeneity in Oligodendrocyte Lineage Maturation and Not Cerebral Blood Flow Predicts Fetal Ovine Periventricular White Matter Injury

Spatial Heterogeneity in Oligodendrocyte Lineage Maturation and Not Cerebral Blood Flow Predicts Fetal Ovine Periventricular White Matter Injury

Maturation-Dependent Vulnerability of Perinatal White Matter in Premature Birth

Causes of Oxidative Stress in the Pre- and Perinatal Period

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