Cornish J D, Dreyer G L, Snyder G E, Kuehl T J, Gerstmann D R, Null D M, Coalson J J, deLemos R A
Department of Pediatrics, Wilford Hall United States Air Force Medical Center, San Antonio, Texas.
Am J Obstet Gynecol. 1994 Jul;171(1):43-9. doi: 10.1016/s0002-9378(94)70075-3.
Our purpose was to determine whether perinatal asphyxia or meconium aspiration, or both, can produce the physiologic and histologic pulmonary vascular changes associated with the meconium aspiration syndrome.
Twenty neonatal baboons were studied in four groups: 1, control; 2, meconium aspiration; 3, asphyxia (intermittent cord compression); and 4, asphyxia with meconium aspiration. Animals were ventilated for 24 hours under ketamine, diazepam, and pancuronium. Data were analyzed by means of mixed model analysis of measures.
Meconium significantly impaired oxygenation (p < 0.001), whereas concurrent asphyxia moderated this effect (p < 0.034). Meconium also increased the need for ventilatory support (p < 0.002). No animal had persistent pulmonary hypertension; neither systemic nor pulmonary systolic pressures differed statistically between the groups. No animal showed evidence of abnormal pulmonary arteriolar muscularization.
Sublethal perinatal asphyxia or meconium aspiration were insufficient to produce either the physiologic or histologic changes of severe meconium aspiration syndrome. It is unlikely that intrapartum fetal distress alone can produce this syndrome in human neonates.
我们的目的是确定围产期窒息或胎粪吸入，或两者兼而有之，是否会产生与胎粪吸入综合征相关的生理和组织学肺血管变化。
对20只新生狒狒进行四组研究：1. 对照组；2. 胎粪吸入组；3. 窒息组（间歇性脐带压迫）；4. 窒息合并胎粪吸入组。动物在氯胺酮、地西泮和泮库溴铵作用下通气24小时。数据采用混合模型测量分析法进行分析。
胎粪显著损害氧合（p < 0.001），而同时存在的窒息减轻了这种影响（p < 0.034）。胎粪还增加了通气支持的需求（p < 0.002）。没有动物出现持续性肺动脉高压；各组之间的体循环和肺循环收缩压在统计学上没有差异。没有动物表现出肺小动脉肌化异常的证据。
亚致死性围产期窒息或胎粪吸入不足以产生严重胎粪吸入综合征的生理或组织学变化。单纯的产时胎儿窘迫不太可能在人类新生儿中产生这种综合征。
