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首页> 外文期刊>Infection and immunity >Tumor necrosis factor alpha-induced pulmonary vascular endothelial injury.
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Tumor necrosis factor alpha-induced pulmonary vascular endothelial injury.

机译：肿瘤坏死因子α诱导的肺血管内皮损伤。

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Tumor necrosis factor alpha (TNF-alpha) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied whether human recombinant TNF-alpha (rTNF-alpha) could increase pulmonary edema formation and pulmonary vascular permeability. Rabbits preinfused with 125I-albumin were administered rTNF-alpha or saline. Animals were sacrificed, and lung wet/dry weight ratios as well as bronchoalveolar lavage fluid and plasma 125I activities were determined. rTNF-alpha increased lung wet/dry weight ratios by 151% (P less than 0.02) and bronchoalveolar lavage fluid/plasma 125I activity ratios by 376% (P less than 0.01) compared with values for saline controls. Electron microscopy of lung sections demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural permeability tracer. To demonstrate that rTNF-alpha could directly increase pulmonary vascular endothelial permeability in vitro, we studied albumin transfer across cultured porcine pulmonary artery endothelial cell monolayers. rTNF-alpha induced time-dependent dose-response increments in transendothelial albumin flux in the absence of granulocyte effector cells. These observations suggest that rTNF-alpha can provoke acute pulmonary vascular endothelial injury in vivo as well as in vitro.
机译：肿瘤坏死因子α（TNF-alpha）介导急性期反应的成分，刺激粒细胞代谢，并诱导内皮细胞表面变化。我们研究了人类重组TNF-α（rTNF-alpha）是否可以增加肺水肿的形成和肺血管通透性。预注入125 I-白蛋白的兔子接受rTNF-α或生理盐水。处死动物，并测定肺湿/干重量比以及支气管肺泡灌洗液和血浆125I活性。与盐水对照组相比，rTNF-alpha使肺湿/干重比增加了151％（P小于0.02），支气管肺泡灌洗液/血浆125I活性比增加了376％（P小于0.01）。肺部电子显微镜检查显示内皮损伤，血管周围水肿和超微结构通透性示踪剂外渗。为了证明rTNF-α可以在体外直接增加肺血管内皮通透性，我们研究了跨培养的猪肺动脉内皮细胞单层的白蛋白转移。在没有粒细胞效应细胞的情况下，rTNF-α诱导的跨内皮白蛋白通量的时间依赖性剂量反应增加。这些观察结果表明，rTNF-α可以在体内和体外引起急性肺血管内皮损伤。

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