DIFFUSE ALVEOLAR DAMAGE IN THE EVOLUTION OF BRONCHOPULMONARY DYSPLASIA IN THE BABOON
DIFFUSE ALVEOLAR DAMAGE IN THE EVOLUTION OF BRONCHOPULMONARY DYSPLASIA IN THE BABOON
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DOI：
10.1203/00006450-198809000-00017
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发表时间：
1988-09-01
影响因子：
3.6
通讯作者：
DELEMOS, RA
中科院分区：
文献类型：
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作者：
COALSON, JJ;KUEHL, TJ;DELEMOS, RA
肺不成熟、氧暴露引起自由基细胞损伤以及机械通气引起的气压伤与支气管肺发育不良的发病机制有关。在成人呼吸窘迫综合征的成人对应物中，弥漫性肺泡损伤是疾病过程中可能发生的肺部发现的组织病理学序列的特征。尽管成人呼吸窘迫综合征有多种病因，但已知氧气暴露升高是导致随后发生的肺损伤的一个因素。在支气管肺发育不良中，氧气暴露被认为是损伤的主要因素。本研究调查了早产狒狒模型的透明膜病/支气管肺发育不良的组织病理学结果的演变，并与患有成年呼吸窘迫综合征的接受氧气治疗的成年狒狒进行比较。对 121 只早产狒狒在产后 0、0.5、1、2、3-6、7-11 天以上的肺部样本进行的研究发现，与人类和成年狒狒相比，早产狒狒的肺部渗出反应延迟且更迟钝。弥漫性肺泡损伤渗出期的主要组织病理学发现是囊性水肿，而不是透明膜，与接受同等治疗的成人肺相比，婴儿肺发生的时间较晚（7-11天），其中最大渗出性变化出现在3-6天。与成年狒狒相比，早产狒狒的修复反应的特点是囊壁增厚和纤维化，囊/肺泡空间的壁内组织较少。早产儿的气道变化比成人疾病更严重。这些发现表明，弥漫性肺泡损伤确实发生在未成熟的肺中，尽管与类似损伤的成年人相比具有不同的特征。
Pulmonary immaturity, oxygen exposure that elicits cellular damage by free radicals, and barotrauma induced by mechanical ventilation are implicated in the pathogenesis of bronchopulmonary dysplasia. In the adult counterpart of adult respiratory distress syndrome, diffuse alveolar damage characteristics a histopathological sequence of lung findings that can occur during the disease course. Although adult respiratory distress syndrome has many etiologies, elevated oxygen exposure is known to be a contributor to the ensuing lung injury. In bronchopulmonary dysplasia, oxygen exposure is thought to be a primary agent of injury. The evolution of the histopathological findings in the premature baboon model of hyaline membrane disease/bronchopulmonary dysplasia was investigated in this study and compared to that in oxygen-treated adult baboons with adult respiratory distress syndrome. Findings from lung specimens of 121 prematurely delivered baboons at 0, 0.5, 1, 2, 3-6, 7-11+ days after delivery document that the premature lung has a delayed and more blunted exudative response when compared to that of human and baboon adults. Saccular edema, not hyaline membranes, is the dominant histopathological finding in the exudative phase of diffuse alveolar damage and occurs later (7-11 days) in infant lungs when compared to comparably treated adult lungs in which maximal exudative changes are seen at 3-6 days. The reparative response in the premature baboon is characterized by saccular wall thickening and fibrosis, with less intramural organization of exudate in saccular/alveolar spaces when compared to adults. The airway changes in the premature are more severe than those seen in adult disease. These findings indicate that diffuse alveolar damage does occur in the immature lung albeit with differing characteristics when contrasted to comparably injured adults.