Perinatal Hypoxemia and Oxygen Sensing.
Perinatal Hypoxemia and Oxygen Sensing.
复制标题
DOI：
10.1002/cphy.c190046
复制
发表时间：
2021-04-01
影响因子：
5.8
通讯作者：
Konduri GG
中科院分区：
文献类型：
--
作者：
Mouradian GC Jr;Lakshminrusimha S;Konduri GG
呼吸控制的发展开始于子宫内，并在出生后继续。胎儿呼吸运动是建立肺和控制呼吸的中枢机制之间的连接所必需的。呼吸控制的成熟，包括缺氧化学敏感性的增加，在出生后继续。氧合不足或缺氧是一种主要的应激源，可以在胎儿和新生儿中表现出不同的原因。虽然胎儿和新生儿有不同的缺氧感应机制，对急性缺氧的反应也不同，但这两种反应都能防止呼吸和其他发育过程的偏离。间歇性和慢性缺氧对正常发育的呼吸过程构成更大的威胁。由于母亲的睡眠呼吸障碍和睡眠呼吸暂停而引起的间歇性缺氧，增加了正常呼吸，减少了与出生后喘息和自动复苏受损相关的缺氧性呼吸反应。由于生物或环境（即高海拔）因素导致的慢性胎儿缺氧与胎儿生长受限和早产有关，导致出生后缺氧性呼吸反应降低，呼吸不规则增加。驱动这些变化的机制包括延迟的化学感受器发育、儿茶酚胺能活性、异常髓鞘形成、背侧呼吸组中星形胶质细胞增殖增加等。长期高海拔居民表现出良好的适应慢性缺氧一样，他们的后代。由于呼吸系统不成熟，新生儿间歇性缺氧在早产儿中很常见，因此，由于缺氧敏感性不足，新生儿呼吸动力降低，呼吸暂停。然而，持续的间歇性缺氧可增强缺氧敏感性，引起呼吸过度，随后发生呼吸暂停;呼吸暂停的数量与早产儿缺氧敏感性的程度呈正相关。慢性新生儿缺氧可能由胎儿并发症（如母亲吸烟）或出生后心血管问题引起，由于颈动脉体纤维对缺氧的反应减弱，导致至少在青春期内缺氧反应减弱，脑干5-羟色胺、小胶质细胞和炎症可能起作用，尽管这些影响取决于慢性缺氧开始的年龄。胎儿和新生儿间歇性和慢性缺氧与早产有关，并通过其对缺氧感应机制的直接影响和对正常发育过程的中断使呼吸系统复杂化。因此，氧稳态的精确调节对于呼吸控制网络的正常发育至关重要。
The development of the control of breathing begins in utero and continues postnatally. Fetal breathing movements are needed for establishing connectivity between the lungs and central mechanisms controlling breathing. Maturation of the control of breathing, including the increase of hypoxia chemosensitivity, continues postnatally. Insufficient oxygenation, or hypoxia, is a major stressor that can manifest for different reasons in the fetus and neonate. Though the fetus and neonate have different hypoxia sensing mechanisms and respond differently to acute hypoxia, both responses prevent deviations to respiratory and other developmental processes. Intermittent and chronic hypoxia pose much greater threats to the normal developmental respiratory processes. Gestational intermittent hypoxia, due to maternal sleep-disordered breathing and sleep apnea, increases eupneic breathing and decreases the hypoxic ventilatory response associated with impaired gasping and autoresuscitation postnatally. Chronic fetal hypoxia, due to biologic or environmental (i.e. high-altitude) factors, is implicated in fetal growth restriction and preterm birth causing a decrease in the postnatal hypoxic ventilatory responses with increases in irregular eupneic breathing. Mechanisms driving these changes include delayed chemoreceptor development, catecholaminergic activity, abnormal myelination, increased astrocyte proliferation in the dorsal respiratory group, among others. Long-term high-altitude residents demonstrate favorable adaptations to chronic hypoxia as do their offspring. Neonatal intermittent hypoxia is common among preterm infants due to immature respiratory systems and thus, display a reduced drive to breathe and apneas due to insufficient hypoxic sensitivity. However, ongoing intermittent hypoxia can enhance hypoxic sensitivity causing ventilatory overshoots followed by apnea; the number of apneas is positively correlated with degree of hypoxic sensitivity in preterm infants. Chronic neonatal hypoxia may arise from fetal complications like maternal smoking or from postnatal cardiovascular problems, causing blunting of the hypoxic ventilatory responses throughout at least adolescence due to attenuation of carotid body fibers responses to hypoxia with potential roles of brainstem serotonin, microglia, and inflammation, though these effects depend on the age in which chronic hypoxia initiates. Fetal and neonatal intermittent and chronic hypoxia are implicated in preterm birth and complicate the respiratory system through their direct effects on hypoxia sensing mechanisms and interruptions to the normal developmental processes. Thus, precise regulation of oxygen homeostasis is crucial for normal development of the respiratory control network.
登录
查看更多内容
影响因子：
3.3
作者：
Bavis, RW;Mitchell, GS
通讯作者：
Mitchell, GS
影响因子：
2.3
作者：
Bavis, Ryan W.;Kim, Insook;Pradhan, Nelish;Nawreen, Nawshaba;Dmitrieff, Elizabeth F.;Carroll, John L.;Donnelly, David F.
通讯作者：
Donnelly, David F.
影响因子：
2.4
作者：
ADZICK, NS;HARRISON, MR;FINKBEINER, W
通讯作者：
FINKBEINER, W
影响因子：
3.1
作者：
Abu-Shaweesh, Jaial M.;Martin, Richard J.
通讯作者：
Martin, Richard J.
影响因子：
9.6
作者：
Angel Martinez-Garcia, Miguel;Campos-Rodriguez, Francisco;Gozal, David
通讯作者：
Gozal, David