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3-甲基吲哚诱导山羊肺损伤。

3-methylindole-induced pulmonary injury in goats.

作者信息

Huang T W, Carlson J R, Bray T M, Bradley B J

出版信息

Am J Pathol. 1977 Jun;87(3):647-66.

Abstract

Ruminal administration of 3-methylindole in goats severe pulmonary edema and respiratory distress. Electron microscopic studies of lungs reveal extensive degeneration and necrosis of alveolar membranous pneumocytes and bronchiolar epithelium. The necrosis of the pneumocytes is followed by proliferation of granular pneumocytes, which repopulate the alveolar basal lamina scaffold. 3-Methylindole may also induce proliferation of smooth endoplasmic reticulum in the remaining membranous pneumocytes and nonciliated columnar cells, indicating that these two cell types are involved in the xenobiotic function of the lung. The results suggest that 3-methylindole in cigarette smoke may play an important role in the pathogenesis of small airway disease and emphysema, and that patients with severe liver diseases or portocaval shunt may be predisposed to diffuse alveolar damage by 3-methylindole produced in the intestinal tract.

摘要

给山羊瘤胃注射3-甲基吲哚会导致严重的肺水肿和呼吸窘迫。肺部的电子显微镜研究显示,肺泡膜性肺细胞和细支气管上皮广泛变性和坏死。肺细胞坏死后,颗粒性肺细胞增殖,重新填充肺泡基底层支架。3-甲基吲哚还可能诱导剩余膜性肺细胞和无纤毛柱状细胞中滑面内质网的增殖,表明这两种细胞类型参与了肺的异生物质功能。结果表明,香烟烟雾中的3-甲基吲哚可能在小气道疾病和肺气肿的发病机制中起重要作用,并且严重肝病或门腔分流患者可能易受肠道产生的3-甲基吲哚导致的弥漫性肺泡损伤影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/2032146/fe1f6bdc4262/amjpathol00400-0192-a.jpg

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