• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

肺泡巨噬细胞对高压一氧化碳暴露的反应。

Pulmonary alveolar macrophage response to hyperbaric carbon monoxide exposure.

作者信息

Roloff M V, D'Addario A P, Buffum E J

出版信息

Undersea Biomed Res. 1978 Mar;5(1):15-23.

PMID:636071
Abstract

The sublethal effects of carbon monoxide (CO) in hyperbaric environments have not been adequately characterized. A physiologically sensitive indicator of sublethal effects of a contaminant is the pulmonary alveolar macrophage (PAM). The guinea pig PAM and its reaction to various CO concentrations at 8 atmospheres absolute (ATA) and the surface-equivalent concentrations at 1 ATA were studied in this experiment. In the absence of CO, PAM counts and viabilites from guinea pigs exposed to a helium-oxygen environment at either 1 or 8 ATA were not significantly different from one another. Mean PAM viability for guinea pigs exposed to CO concentrations at 2250--4200 mg/m3 at 8 ATA was 68.4 +/- 7.3% and was not significantly different from the 1-ATA viability value of 72.0 +/- 4.5% for the 1600--4200 mg/m3 CO range. The data show that at 1 to 8 ATA and CO concentrations of 1600--4200 mg/m3, the decrease in PAM viability was accompanied by dramatic five- to sixfold increases in PAM counts.

摘要

高压环境中一氧化碳(CO)的亚致死效应尚未得到充分描述。污染物亚致死效应的一个生理敏感指标是肺泡巨噬细胞(PAM)。本实验研究了豚鼠PAM及其在8个绝对大气压(ATA)下对各种CO浓度以及1个ATA下表面等效浓度的反应。在没有CO的情况下,暴露于1或8个ATA的氦氧环境中的豚鼠的PAM计数和活力彼此之间没有显著差异。暴露于8个ATA下2250--4200 mg/m3 CO浓度的豚鼠的平均PAM活力为68.4 +/- 7.3%,与1600--4200 mg/m3 CO范围内1个ATA活力值72.0 +/- 4.5%没有显著差异。数据表明,在1至8个ATA以及1600--4200 mg/m3的CO浓度下,PAM活力的降低伴随着PAM计数急剧增加五到六倍。

相似文献

1
Pulmonary alveolar macrophage response to hyperbaric carbon monoxide exposure.肺泡巨噬细胞对高压一氧化碳暴露的反应。
Undersea Biomed Res. 1978 Mar;5(1):15-23.
2
Effects of Diesel engine exhaust on pulmonary alveolar macrophages.柴油机尾气对肺泡巨噬细胞的影响。
Scan Electron Microsc. 1980(3):327-38.
3
Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats.高压氧对一氧化碳介导的大鼠脑损伤中白细胞B2整合素的功能抑制作用
Toxicol Appl Pharmacol. 1993 Dec;123(2):248-56. doi: 10.1006/taap.1993.1243.
4
NTP Toxicology and Carcinogenesis Studies of Nickel Subsulfide (CAS No. 12035-72-2) in F344 Rats and B6C3F1 Mice (Inhalation Studies).硫化镍(CAS编号:12035-72-2)对F344大鼠和B6C3F1小鼠的NTP毒理学和致癌性研究(吸入研究)
Natl Toxicol Program Tech Rep Ser. 1996 Jul;453:1-365.
5
On half-clearance time of carbon monoxide hemoglobin in blood during hyperbaric oxygen therapy (OHP).高压氧治疗期间血液中碳氧血红蛋白的半清除时间。
Bull Tokyo Med Dent Univ. 1975 Mar;22(1):63-77.
6
Deactivation of guinea pig pulmonary alveolar macrophage responses to N-formyl-methionyl-leucyl-phenylalanine: chemotaxis, superoxide generation, and binding.豚鼠肺泡巨噬细胞对N-甲酰甲硫氨酰亮氨酰苯丙氨酸反应的失活:趋化性、超氧化物生成及结合
J Immunol. 1985 Mar;134(3):1823-6.
7
Ketamine and thiopental sleep responses in guinea pigs in hyperbaric helium-oxygen.
Undersea Biomed Res. 1979 Dec;6(4):329-38.
8
Enhanced proliferation of pulmonary alveolar macrophages after carbon instillation in mice depleted of blood monocytes by strontium-89.用锶-89清除血液单核细胞的小鼠在注入碳后肺泡巨噬细胞增殖增强。
Lab Invest. 1986 Feb;54(2):154-9.
9
Cytotoxic effects of hydrogen sulfide on pulmonary alveolar macrophages in rats.硫化氢对大鼠肺泡巨噬细胞的细胞毒性作用。
J Toxicol Environ Health. 1991 May;33(1):57-64. doi: 10.1080/15287399109531505.
10
NTP Toxicology and Carcinogenesis Studies of Nickel Sulfate Hexahydrate (CAS No. 10101-97-0) in F344 Rats and B6C3F1 Mice (Inhalation Studies).六水合硫酸镍(CAS编号:10101-97-0)在F344大鼠和B6C3F1小鼠中的NTP毒理学与致癌性研究(吸入研究)
Natl Toxicol Program Tech Rep Ser. 1996 Jul;454:1-380.

引用本文的文献

1
Alterations in macrophage functions by environmental chemicals.环境化学物质对巨噬细胞功能的影响。
Environ Health Perspect. 1984 Apr;55:343-58. doi: 10.1289/ehp.8455343.