Application of a neuroscience research model to study neuroprotection in children with congenital heart disease.
Application of a neuroscience research model to study neuroprotection in children with congenital heart disease.
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应用神经科学研究模型研究先天性心脏病儿童的神经保护。
DOI:
10.1016/j.jtcvs.2018.06.067
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发表时间:
2018
期刊:
影响因子:
--
通讯作者:
Jonas,RichardA
中科院分区:
文献类型:
--
作者:
Ishibashi,Nobuyuki;Jonas,RichardA
Over the past 10 to 20 years, it has become clear that neurologic deficits associated with congenital heart disease (CHD) are not simply a consequence of surgery and exposure to cardiopulmonary bypass. The causes are in fact cumulative and multifactorial. 1 They include prenatal events such as genetic alterations such as ubiquitous copy number variants or disturbances of fetal cerebral blood flow. 2, 3 Brain development is often delayed in a fetus with CHD resulting in an immature brain even in a newborn infant born at full term. And an immature brain appears to be exquisitely susceptible to the inflammation (eg, systemic inflammatory response syndrome) and hypoxia/ischemia that can be a consequence of surgery. 4 It is possible that current management strategies of cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) that are optimal for protection in a normally developing brain are damaging to a brain with immaturity and preoperative injury.Huang and colleagues5 from Shanghai Children’s Medical Center describe an innovative study using temperature-controlled neonatal rat brain slices exposed to oxygen glucose deprivation to simulate DHCA. The authors found that injury to preoligodendrocytes could be reduced either by deep hypothermia or application of minocycline. Injury to preoligodendrocytes is clinically relevant to cardiac surgeons because it can result in white matter injury that has been a signature insult observed in babies with CHD before surgery with exacerbation after surgery. White matter injury can become manifest as motor deficits, such as incoordination, as well as behavior problems such as attention deficit hyperactivity disorder, similar to the problems seen in ultrapremature populations.
影响因子:
20.1
作者:
Morton PD;Ishibashi N;Jonas RA
通讯作者:
Jonas RA
影响因子:
158.5
作者:
Miller, Steven P.;McQuillen, Patrick S.;Vigneron, Daniel B.
通讯作者:
Vigneron, Daniel B.
影响因子:
37.8
作者:
Beca, John;Gunn, Julia K.;Shekerdemian, Lara S.
通讯作者:
Shekerdemian, Lara S.