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子宫内慢性低氧血症对大鼠新生儿肺动脉结构的影响。

Effects of chronic in utero hypoxemia on rat neonatal pulmonary arterial structure.

作者信息

Geggel R L, Aronovitz M J, Reid L M

出版信息

J Pediatr. 1986 May;108(5 Pt 1):756-9. doi: 10.1016/s0022-3476(86)81060-5.

Abstract

Idiopathic persistent pulmonary hypertension of the newborn infant (PPHN) is characterized by intrauterine structural remodeling of the pulmonary arterial bed, consisting of precocious development of muscle in intraacinar arteries, proliferation of adventitial connective tissue, and sometimes medial hypertrophy of preacinar arteries. To evaluate whether gestational hypoxemia causes these changes, we studied pulmonary arterial structure in two groups of newborn rats: one control, the other exposed to hypoxemia produced by maternal hypoxia during the second half of gestation. Morphometric analysis of the pulmonary arterial bed was performed after barium injection into the pulmonary arteries and formol saline expansion of the air spaces. Birth weight was similar in each group. Hematocrit was elevated in the hypoxemia group (51% +/- 1.0% vs 46% +/- 0.8%, P less than 0.005). The structure of preacinar and intraacinar arteries was similar and normal in both groups. Chronic fetal hypoxemia in the rat does not produce the pulmonary arterial structural changes identified in fatal cases of PPHN in human infants.

摘要

新生儿特发性持续性肺动脉高压(PPHN)的特征是肺动脉床的子宫内结构重塑,包括腺泡内动脉肌肉的早熟发育、外膜结缔组织的增殖,有时还包括腺泡前动脉的中层肥厚。为了评估孕期低氧血症是否会导致这些变化,我们研究了两组新生大鼠的肺动脉结构:一组为对照组,另一组在孕期后半期暴露于由母体缺氧产生的低氧血症环境中。在向肺动脉注射钡剂并对气腔进行甲醛生理盐水扩张后,对肺动脉床进行形态计量分析。每组的出生体重相似。低氧血症组的血细胞比容升高(51%±1.0%对46%±0.8%,P<0.005)。两组腺泡前和腺泡内动脉的结构相似且正常。大鼠慢性胎儿低氧血症不会产生在人类婴儿PPHN致命病例中所发现的肺动脉结构变化。

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