Sustained inflation at birth did not protect preterm fetal sheep from lung injury
Sustained inflation at birth did not protect preterm fetal sheep from lung injury
复制标题
DOI：
10.1152/ajplung.00162.2013
复制
发表时间：
2013-09-01
影响因子：
4.9
通讯作者：
Jobe, Alan H.
中科院分区：
文献类型：
--
作者：
Hillman, Noah H.;Kemp, Matthew W.;Jobe, Alan H.
出生时持续的肺膨胀(SI)可能会招募功能性残气量(FRC)。临床上，SI增加了早产儿的氧合，减少了插管需求。我们测试了SI来招募FRC是否可以减少胎儿、早产羔羊随后的机械通气所造成的肺损伤。将早产儿(孕128+/-1天)从子宫外取出，行气管切开术，取出胎肺积液。在维持胎盘循环的同时，胎儿被随机分为4组：1)呼气末正压(PEEP)8cmH(2)O(n=4)，2)S SI至50cmH(2)O，然后PEEP 8cmH(2)O(n=10)，3)机械通气潮气量(VT)7ml/kg(n=13)，或4)20 S SI然后VT 7ml/kg(n=13)。羔羊用95%N-2/5%CO2和PEEP 8 CMH(2)O进行呼吸，在SI期间测量容量募集，并在额外的胎盘支持30分钟后收集胎儿组织。SI的平均FRC募集量为15毫升/公斤(范围8-27)。最终FRC的50%由2名S完成，65%由5名S完成，90%由15名S完成，这表明招募FRC需要延长SI时间。SI单独将急性时相蛋白释放到胎儿肺液中，并增加肺内促炎症细胞因子和急性时相反应基因的mRNA表达。机械通气进一步增加了肺损伤的所有标志物。无论使用多少FRC，机械通气前的SI均不会改变出生时机械通气的急性期和促炎反应。
Sustained lung inflations (SI) at birth may recruit functional residual capacity (FRC). Clinically, SI increase oxygenation and decrease need for intubation in preterm infants. We tested whether a SI to recruit FRC would decrease lung injury from subsequent ventilation of fetal, preterm lambs. The preterm fetus (128 +/- 1 day gestation) was exteriorized from the uterus, a tracheostomy was performed, and fetal lung fluid was removed. While maintaining placental circulation, fetuses were randomized to one of four 15-min interventions: 1) positive end-expiratory pressure (PEEP) 8 cmH(2)O (n = 4), 2) 20 s SI to 50 cmH(2)O then PEEP 8 cmH(2)O (n = 10), 3) mechanical ventilation at tidal volume (VT) 7 ml/kg (n = 13), or 4) 20 s SI then ventilation at VT 7 ml/kg (n = 13). Lambs were ventilated with 95% N-2/5% CO2 and PEEP 8 cmH(2)O. Volume recruitment was measured during SI, and fetal tissues were collected after an additional 30 min on placental support. SI achieved a mean FRC recruitment of 15 ml/kg (range 8-27). Fifty percent of final FRC was achieved by 2 s, 65% by 5 s, and 90% by 15 s, demonstrating prolonged SI times are needed to recruit FRC. SI alone released acute-phase proteins into the fetal lung fluid and increased mRNA expression of proinflammatory cytokines and acute-phase response genes in the lung. Mechanical ventilation further increased all markers of lung injury. SI before ventilation, regardless of the volume of FRC recruited, did not alter the acute-phase and proinflammatory responses to mechanical ventilation at birth.