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小鼠减压性骨坏死

Dysbaric osteonecrosis in mice.

作者信息

Chryssanthou C P

出版信息

Undersea Biomed Res. 1976 Jun;3(2):67-83.

PMID:951827
Abstract

The histopathology of dysbaric osteonecrosis and the influence of the number of exposures, compression rate, and obesity on the incidence and latency of the lesion were studied in 438 mice (2505 bones were examined). The animals were subjected to 75 psig air pressure for 2-6 hours (single or multiple exposures). Compression was rapid or stage. Decompression was safe. Osteonecrosis developed in the epiphysis of the tibia and/or femur in 34.1% of obese and in 5.8% of thin animals after a latent period of 2 to at least 12 months. It was concluded that: 1. dysbaric osteonecrosis appears to be independent of decompression sickness; 2. in obese mice the incidence is higher and the latent period shorter; 3. multiple exposures result in higher incidence and earlier lesions than single exposure; 4. the incidence is lower with stage than with rapid compression; 5. the pathogenesis of osteonecrosis may involve several factors (circulatory impairment by extravascular or intravascular bubbles, emboli, thrombi, vasoactive substances, gas-induced osmosis, autoimmunity) acting in concert or in sequence.

摘要

对438只小鼠(检查了2505块骨骼)进行了减压性骨坏死的组织病理学研究,以及暴露次数、压缩速率和肥胖对病变发生率和潜伏期的影响。动物接受75磅/平方英寸的气压2至6小时(单次或多次暴露)。压缩为快速或分阶段进行。减压是安全的。在2至至少12个月的潜伏期后,34.1%的肥胖动物和5.8%的瘦动物在胫骨和/或股骨骨骺出现骨坏死。得出以下结论:1. 减压性骨坏死似乎与减压病无关;2. 在肥胖小鼠中,发病率更高,潜伏期更短;3. 多次暴露比单次暴露导致更高的发病率和更早的病变;4. 分阶段压缩的发病率低于快速压缩;5. 骨坏死的发病机制可能涉及多种因素(血管外或血管内气泡、栓子、血栓、血管活性物质、气体诱导的渗透、自身免疫引起的循环障碍)协同或相继作用。

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