Peters C A, Docimo S G, Luetic T, Reid L M, Retik A B, Mandell J
Department of Surgery, Children's Hospital, Boston, Massachusetts 02115.
J Urol. 1991 Oct;146(4):1178-83. doi: 10.1016/s0022-5347(17)38035-7.
A model of early gestation bladder outlet obstruction and oligohydramnios in the fetal lamb is characterized by small, immature lungs (pulmonary hypoplasia). The current study examines how in utero relief of urinary tract obstruction produced early in gestation modifies pulmonary hypoplasia. Bladder obstruction was created at 60 days gestation in fetal sheep (term = 140 days); 11 fetuses then underwent in utero decompression at 95 to 100 days; six were left obstructed. Five normal fetuses served as controls and two underwent sham obstruction and vesicostomy. All were delivered and sacrificed near term (135 days), the right lung was inflation-fixed and its volume determined. Relative volumes of alveoli, alveolar ducts, and tissue, alveolar surface area, and alveolar numerical density were estimated morphometrically. Kidneys were examined histologically. In all animals persistent bladder obstruction produced oligohydramnios. Bladder obstruction to term produced pulmonary hypoplasia with a mean right lung volume-to-body weight ratio (LV:BW) of 14.3 cc./kg. (normal = 36.4, p less than 0.001). Structural immaturity was evidenced by an airspace fraction of only 57% (normal = 68%, p less than 0.05). Kidneys in these animals were not dysplastic; there was hydronephrosis or evidence of spontaneous urinary decompression. In eight of the 11 animals, decompression improved the LV:BW ratio to 28.4 cc./kg. (vs. obstructed, p less than 0.001; vs normal, p less than 0.05) and normalized maturity. All had increased amniotic fluid at delivery; kidneys in 7/8 animals were normal, and the other had moderate hydronephrosis. One of the 11 animals had normal kidneys, oligohydramnios, immature lungs, but with normal volume. Oligohydramnios was present in the other two of 11 fetuses despite successful decompression and they had markedly dysmorphic kidneys and profoundly hypoplastic and immature lungs (LV:BW 5.1 cc./kg.). Even after 35 days (25% gestation) of obstruction, in utero urinary tract decompression permits better lung growth and maturation than in persistently obstructed animals. The degree of renal damage from obstruction appears to be a critical determinant in the correction of pulmonary hypoplasia.
妊娠早期膀胱出口梗阻和羊水过少的胎羊模型的特点是肺小且未成熟（肺发育不全）。本研究探讨妊娠早期宫内解除尿路梗阻如何改变肺发育不全。在妊娠60天给胎羊造成膀胱梗阻（足月为140天）；11只胎儿在95至100天接受宫内减压；6只保持梗阻状态。5只正常胎儿作为对照，2只接受假梗阻和膀胱造瘘术。所有胎儿均在足月（135天）时分娩并处死，右肺充气固定并测定其体积。通过形态计量学估计肺泡、肺泡管和组织的相对体积、肺泡表面积和肺泡数量密度。对肾脏进行组织学检查。在所有动物中，持续性膀胱梗阻导致羊水过少。梗阻至足月导致肺发育不全，右肺体积与体重比（LV:BW）平均为14.3立方厘米/千克（正常为36.4，p<0.001）。结构不成熟表现为气腔分数仅为57%（正常为68%，p<0.05）。这些动物的肾脏没有发育异常；有肾盂积水或自发尿路减压的证据。11只动物中的8只，减压后LV:BW比值提高到28.4立方厘米/千克（与梗阻组相比，p<0.001；与正常组相比，p<0.05），成熟度恢复正常。所有动物分娩时羊水都增加了；8只动物中的7只肾脏正常，另一只患有中度肾盂积水。11只动物中的1只肾脏正常，羊水过少，肺未成熟，但体积正常。11只胎儿中的另外2只尽管成功减压仍存在羊水过少，且肾脏明显畸形，肺严重发育不全且未成熟（LV:BW为5.1立方厘米/千克）。即使梗阻35天（妊娠25%）后，宫内尿路减压也比持续梗阻的动物能使肺更好地生长和成熟。梗阻造成的肾损伤程度似乎是纠正肺发育不全的关键决定因素。
