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支气管肺发育不良(BPD)中的气道病变与超氧化物歧化酶(SOD)分布

Airway lesions and superoxide dismutase (SOD) distribution in bronchopulmonary dysplasia (BPD).

作者信息

Ohbayashi C, Kanomata N, Hanioka K, Itoh H

机构信息

Department of Pathology, Hyogo Prefectural Kakogawa Hospital, Japan.

出版信息

Kobe J Med Sci. 1997 Oct;43(5):191-211.

PMID:9642974
Abstract

We examined 71 cases of bronchopulmonary dysplasia (BPD) at autopsy and divided them into five groups on the basis of the patients' survival time, studying on the histological changes in the airways for the purpose of clarifying the pathogenesis of BPD from hyaline membrane disease (HMD). Furthermore, bronchiolar occlusion was classified into four types: secretion, obliterative bronchiolitis, intraluminal plug, and hyperplasia of bronchiolar components. The same occlusive findings as in bronchioli and hyaline membrane were observed from respiratory bronchioles to alveolar ducts. However, there was no obvious correlation between airway lesions and accompanying alveolar lesions excepts three cases of obliterative bronchiolitis. Furthermore, immunohistochemical studies with anti-human SOD antibodies were performed. Mn-SOD was positive for alveolar macrophages in longer surviving infants without significant correlation with histological variation, whereas slightly positive or negative in infants who died within 1 week; CuZn-SOD was rarely positive in any cases. These results is highly correlated to the pathogenesis of BPD and to its pathological advancement with its clinical course.

摘要

我们对71例支气管肺发育不良(BPD)病例进行了尸检,并根据患者的存活时间将其分为五组,研究气道的组织学变化,以阐明BPD源自透明膜病(HMD)的发病机制。此外,细支气管闭塞分为四种类型:分泌物、闭塞性细支气管炎、管腔内栓子和细支气管成分增生。从呼吸性细支气管到肺泡管均观察到与细支气管和透明膜相同的闭塞性表现。然而,除三例闭塞性细支气管炎外,气道病变与伴随的肺泡病变之间无明显相关性。此外,我们还进行了抗人超氧化物歧化酶(SOD)抗体的免疫组化研究。在存活时间较长的婴儿中,锰超氧化物歧化酶(Mn-SOD)在肺泡巨噬细胞中呈阳性,与组织学变化无显著相关性,而在1周内死亡的婴儿中呈弱阳性或阴性;铜锌超氧化物歧化酶(CuZn-SOD)在任何病例中均很少呈阳性。这些结果与BPD的发病机制及其病理进展与临床病程高度相关。

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