Davidson S, Gil-Ad I, Rogovin H, Laron Z, Reisner S H
Am J Dis Child. 1987 Feb;141(2):145-8. doi: 10.1001/archpedi.1987.04460020035022.
Twenty-nine premature infants were studied to determine whether neonatal asphyxia, apnea, and low blood pressure in the first day of life are associated with elevated plasma beta-endorphin concentrations. Plasma beta-endorphin levels were determined at 0.5 to 2, 4 to 6, and 18 to 24 hours of life, using radioimmunoassay. Premature infants with moderate or severe asphyxia (n = 19) had higher levels at 0.5 to 2 hours of age (32.1 +/- 6.7 vs 16.4 +/- 7.4 pmol/L) and significantly higher levels at 4 to 6 hours of age (50.4 +/- 10.0 vs 22.9 +/- 9.2 pmol/L) compared with the ten nonasphyxiated premature infants. A significant elevation in levels at age 0.5 to 2 hours (39.4 +/- 9.9 vs 17.7 +/- 4.4 pmol/L) and age 4 to 6 hours (59.3 +/- 13.8 vs 27.1 +/- 17.1 pmol/L) was observed in premature infants with low blood pressure or impaired perfusion (n = 12) who required the administration of volume expanders. No differences were observed in premature infants with and without apnea. It may be speculated that the increased endogenous release of beta-endorphins in response to perinatal asphyxia may play a role in the pathogenesis of shock observed in the first day of life.
对29名早产儿进行了研究,以确定出生第一天的新生儿窒息、呼吸暂停和低血压是否与血浆β-内啡肽浓度升高有关。采用放射免疫分析法在出生后0.5至2小时、4至6小时和18至24小时测定血浆β-内啡肽水平。与10名未窒息的早产儿相比,中度或重度窒息的早产儿(n = 19)在0.5至2小时龄时血浆β-内啡肽水平更高(32.1±6.7对16.4±7.4 pmol/L),在4至6小时龄时显著更高(50.4±10.0对22.9±9.2 pmol/L)。在需要使用扩容剂的低血压或灌注受损的早产儿(n = 12)中,观察到在0.5至2小时龄(39.4±9.9对17.7±4.4 pmol/L)和4至6小时龄(59.3±13.8对27.1±17.1 pmol/L)时血浆β-内啡肽水平显著升高。有呼吸暂停和无呼吸暂停的早产儿之间未观察到差异。可以推测,围产期窒息导致β-内啡肽内源性释放增加可能在出生第一天观察到的休克发病机制中起作用。