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缺镁大鼠应激诱导的肺部病变。光镜和电镜研究。

Pulmonary lesion induced by stress in magnesium-deficient rats. A light- and electron-microscopic study.

作者信息

Caddell J L, Blanchette-Mackie E J, Snowden K I, Jackson N N

出版信息

Am J Pathol. 1987 Jun;127(3):430-40.

Abstract

A light- and electron-microscopic study was made of the lungs of magnesium (Mg)-sufficient and Mg-deficient pathogen-free weanling rats raised in a gnotobiotic environment. Mg-sufficient rats were studied unstressed, after mild auditory stress, or after strychnine seizures and showed essentially no pulmonary pathology. Mg-deficient rats were studied with no known seizures or immediately after audiogenic seizure-shock. Light microscopy of lung from Mg-deficient rats with audiogenic seizure-shock revealed atelectasis, generalized edema and hemorrhage, and pleural petechiae. Ultrastructural changes in lung alveoli of Mg-deficient rats with seizure-shock included gaps in capillary endothelium, swelling and separation of endothelial cells from the underlying basement membranes; Type I cell necrosis and separation from basement membranes; and intraalveolar red blood cells, fibrin, and precipitated plasma. The seizure-shock episode of acute Mg deficiency produces structural changes in the lung similar to changes produced by several forms of shock, early acute oxygen toxicity, and the respiratory distress syndrome (RDS) in human neonates.

摘要

对在悉生环境中饲养的镁(Mg)充足和缺镁的无菌断奶大鼠的肺部进行了光镜和电镜研究。对镁充足的大鼠在无应激状态下、轻度听觉应激后或士的宁惊厥后进行研究,结果显示基本无肺部病理变化。对缺镁大鼠在无已知惊厥发作时或在听源性惊厥休克后立即进行研究。光镜检查发现,经历听源性惊厥休克的缺镁大鼠的肺部出现肺不张、全身性水肿和出血,以及胸膜瘀点。经历惊厥休克的缺镁大鼠肺泡的超微结构变化包括毛细血管内皮细胞间隙、内皮细胞肿胀并与下方基底膜分离;I型细胞坏死并与基底膜分离;以及肺泡内红细胞、纤维蛋白和沉淀的血浆。急性缺镁的惊厥休克发作会在肺部产生结构变化,类似于几种形式的休克、早期急性氧中毒以及人类新生儿呼吸窘迫综合征(RDS)所产生的变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbb7/1899770/a671dda2a378/amjpathol00147-0035-a.jpg

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