Karamanoukian H L, Glick P L, Wilcox D T, Rossman J E, Holm B A, Morin F C
Buffalo Institute of Fetal Therapy (BIFT), Children's Hospital of Buffalo, State University of New York at Buffalo 14222.
J Pediatr Surg. 1995 Jan;30(1):1-4. doi: 10.1016/0022-3468(95)90596-0.
The pathophysiology of the lamb model of congenital diaphragmatic hernia (CDH) involves pulmonary hypoplasia, pulmonary hypertension, and surfactant deficiency. Inhaled nitric oxide (NO) is a highly selective pulmonary vasodilator. The aim of this study was to determine the effects of inhaled NO on pulmonary gas exchange, acid-base balance, and pulmonary pressures in a lamb model of CDH with or without exogenous surfactant therapy. At the gestational age of 78 days (full term, 145 days) 11 lamb fetuses had a diaphragmatic hernia created via a left thoracotomy and then were allowed to continue development in utero. After cesarean section, performed at term, six lambs received exogenous surfactant therapy (50 mg/kg, Infasurf) and five served as controls. All animals were pressure-ventilated for 30 minutes and then received 80 ppm of inhaled NO at an F1O2 of .9 for a 10-minute interval. Compared with the control lambs, the lambs with exogenous surfactant therapy had higher pH (7.17 +/- .06 v 6.96 +/- .07; P < .05), lower PCO2 (73 +/- 8 v 122 +/- 20, p < .05), and higher PO2 (153 +/- 38 v 50 +/- 23; P < .05). In control CDH lambs (without surfactant), inhaled NO did not improve pH, PCO2, or PO2, or decrease pulmonary artery pressure. In CDH lambs given exogenous surfactant, NO decreased pulmonary artery pressures (42 +/- 4 v 53 +/- 5; P < .005) and further improved PCO2 and PO2. NO also made the difference between pulmonary and systemic artery pressures more negative in the surfactant-treated lambs (-15 +/- 4 v -2.3 +/- 2.4; P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)
先天性膈疝（CDH）羔羊模型的病理生理学涉及肺发育不全、肺动脉高压和表面活性剂缺乏。吸入一氧化氮（NO）是一种高度选择性的肺血管扩张剂。本研究的目的是确定在接受或未接受外源性表面活性剂治疗的CDH羔羊模型中，吸入NO对肺气体交换、酸碱平衡和肺压力的影响。在妊娠78天（足月为145天）时，11只羔羊胎儿通过左胸切开术制造膈疝，然后在子宫内继续发育。足月剖宫产术后，6只羔羊接受外源性表面活性剂治疗（50mg/kg，Infasurf），5只作为对照。所有动物进行压力通气30分钟，然后在F1O2为0.9的条件下接受80ppm吸入NO，持续10分钟。与对照羔羊相比，接受外源性表面活性剂治疗的羔羊pH值更高（7.17±0.06对6.96±0.07；P<0.05），PCO2更低（73±8对122±20，P<0.05），PO2更高（153±38对50±23；P<0.05）。在对照CDH羔羊（未使用表面活性剂）中，吸入NO未改善pH值、PCO2或PO2，也未降低肺动脉压力。在给予外源性表面活性剂的CDH羔羊中，NO降低了肺动脉压力（42±4对53±5；P<0.005），并进一步改善了PCO2和PO2。NO还使表面活性剂治疗的羔羊肺与体动脉压力差更负（-15±4对-2.3±2.4；P<0.005）。（摘要截短于250字）
