van Bel F, Dorrepaal C A, Benders M J, Zeeuwe P E, van de Bor M, Berger H M
Department of Pediatrics, University Hospital of Leiden, The Netherlands.
Pediatrics. 1993 Sep;92(3):365-72.
To investigate whether or not postasphyctic cerebral hypoperfusion and decreased cerebral metabolism occur in the perinatally asphyxiated neonate, as has been reported in adults and newborn animals.
Using near-infrared spectroscopy, we monitored changes in oxyhemoglobin (HbO2), deoxyhemoglobin (HbR), total hemoglobin (HbO2 + HbR, which represents changes in cerebral blood volume [CBV]), and cytochrome oxidase (Cytaa3, which indicates changes in oxidation level of this intracerebral mitochondrial enzyme). Thirty-one neonates (gestational age > 34 weeks), divided into three groups, were monitored between 2 and 12 hours or between 12 and 24 hours of life. Group I consisted of healthy newborns: N = 8 (2 to 12 hours) and N = 5 (12 to 24 hours). Patients in group II were moderately asphyxiated newborns but neurologically normal in the first 24 hours of life: N = 6 (2 to 12 hours) and N = 3 (12 to 24 hours). Group III consisted of severely asphyxiated newborns with an abnormal neurologic behavior within 24 hours after birth: N = 5 (2 to 12 hours) and N = 4 (12 to 24 hours).
From 2 to 12 h, CBV levels in groups I and II were stable. In group III CBV decreased in all infants. This decrease in CBV was associated with a drop in both HbO2 and HbR. Cytaa3 was stable in groups I and II, but showed a marked decrease in two of the five infants of group III. There was a positive relationship between CBV and mean arterial blood pressure in groups II and III. Between 12 and 24 hours, all groups showed stable CBV and Cytaa3 patterns. A positive relation existed now between transcutaneous PCO2 and CBV in groups II and III.
CBV, HbO2, HbR, and Cytaa3 decreased in the first 12 hours of life in severely asphyxiated neonates who subsequently developed neurologic abnormalities. We therefore suggest that posthypoxic-ischemic reperfusion injury of the brain during early neonatal life occurs in neonates with severe birth asphyxia.
研究围产期窒息新生儿是否会像成人和新生动物那样发生窒息后脑灌注不足和脑代谢降低。
我们使用近红外光谱法监测了氧合血红蛋白（HbO2）、脱氧血红蛋白（HbR）、总血红蛋白（HbO2 + HbR，代表脑血容量[CBV]的变化）和细胞色素氧化酶（Cytaa3，表明这种脑内线粒体酶氧化水平的变化）的变化。31例胎龄大于34周的新生儿被分为三组，在出生后2至12小时或12至24小时进行监测。第一组为健康新生儿：N = 8（2至12小时）和N = 5（12至24小时）。第二组为中度窒息新生儿，但在出生后24小时内神经功能正常：N = 6（2至12小时）和N = 3（12至24小时）。第三组为出生后24小时内出现神经行为异常的重度窒息新生儿：N = 5（2至12小时）和N = 4（12至24小时）。
在2至12小时内，第一组和第二组的CBV水平稳定。第三组所有婴儿的CBV均下降。CBV的这种下降与HbO2和HbR的下降相关。第一组和第二组的Cytaa3稳定，但第三组五名婴儿中有两名的Cytaa3显著下降。第二组和第三组中CBV与平均动脉血压之间存在正相关关系。在12至24小时之间，所有组的CBV和Cytaa3模式均稳定。第二组和第三组中，经皮PCO2与CBV之间现在存在正相关关系。
随后出现神经异常的重度窒息新生儿在出生后12小时内CBV、HbO2、HbR和Cytaa3均下降。因此，我们认为严重出生窒息的新生儿在新生儿早期会发生缺氧缺血性再灌注脑损伤。
