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自发死亡或从惊厥-休克发作中自发恢复后死亡的缺镁断奶大鼠肺部的结构变化。婴儿猝死综合征的可能方法。

Structural changes in lungs of magnesium-deficient weanling rats dying spontaneously or after spontaneous recovery from the seizure-shock episode. Possible methods for sudden infant death syndromes.

作者信息

Caddell J L, Blanchette-Mackie E J

机构信息

Section of Disorders of Carbohydrate Metabolism, National Institute of Child Health and Human Development, Bethesda, Md.

出版信息

Magnesium. 1988;7(4):195-209.

PMID:3244282
Abstract

A light and electron microscopic study of Mg-deficient weanling rats showed structural changes of the lungs associated with the audiogenic seizure-shock episode, and with sudden, spontaneous death or spontaneous recovery after the shock episode. Pathogen-free weanling males were fed a Mg-deficient (Mg-0) or Mg-sufficient (Mg-100) diet and were raised in a gnotobiotic environment. Mg-100 rats (n = 16), unstressed or stressed with noise or strychnine, showed normal lungs. Mg-0 rats (n = 20) experienced audiogenic seizure-shock, followed by hyperventilation with tonic-clonic hyperextension of the back and extremities. The lungs of Mg-0 rats sacrificed during shock showed marked hemorrhage, including petechiae; edema; and atelectasis. Eight that died after a post-shock period of hyperventilation and hyperextension of the spine showed partial recovery of the pulmonary lesion; they showed well-expanded lungs, pleural petechiae, persistent congestion, with mild to moderate pathology. Mg-0 rats killed for study 2 days after the seizure-shock episode showed few small areas of residual lung pathology. Ultrastructural changes after Mg-O shock included aggregated platelets, leukocytes, and occasional reticulocytes in congested capillaries. Surfactant was disrupted during Mg-0 seizure-shock, but a layer closely applied to the surface of the epithelium was evident 2 days after shock. Mg-0 rats dying spontaneously showed nonspecific structural changes of the lung similar to changes reported in the sudden infant death syndrome (SIDS).

摘要

对缺镁断乳大鼠进行的光镜和电镜研究表明,肺的结构变化与听源性惊厥-休克发作以及休克发作后的突然自发死亡或自发恢复有关。无特定病原体的断乳雄性大鼠被喂食缺镁(Mg-0)或镁充足(Mg-100)的饮食,并在无菌环境中饲养。Mg-100组大鼠(n = 16),无论未受应激还是受到噪音或士的宁应激,肺均正常。Mg-0组大鼠(n = 20)经历听源性惊厥-休克,随后出现过度通气,背部和四肢强直-阵挛性过度伸展。在休克期间处死的Mg-0组大鼠的肺显示出明显的出血,包括瘀点;水肿;和肺不张。8只在休克后出现过度通气和脊柱过度伸展后死亡的大鼠,其肺部病变有部分恢复;它们的肺膨胀良好,有胸膜瘀点、持续充血,病理改变为轻度至中度。在惊厥-休克发作后2天处死用于研究的Mg-0组大鼠,残留的肺部病理改变仅为少数小区域。Mg-0组休克后的超微结构变化包括充血毛细血管内聚集的血小板、白细胞和偶尔出现的网织红细胞。在Mg-0组惊厥-休克期间表面活性物质遭到破坏,但休克后2天可见一层紧密贴附于上皮表面。自发死亡的Mg-0组大鼠肺部显示出非特异性结构变化,类似于婴儿猝死综合征(SIDS)中报道的变化。

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