Granulocyte colony-stimulating factor does not enhance endotoxin-induced acute lung injury in guinea pigs.

Granulocyte colony-stimulating factor does not enhance endotoxin-induced acute lung injury in guinea pigs.
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粒细胞集落刺激因子不会增强内毒素诱导的豚鼠急性肺损伤。

DOI:
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发表时间:
1992
期刊:
American Review of Respiratory Disease
影响因子:
--
通讯作者:
T. Yokoyama
T. Yokoyama
中科院分区:
--
文献类型:
--
作者:
M. Kanazawa;A. Ishizaka;N. Hasegawa;Yukio Suzuki;T. Yokoyama

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我们研究了重组人粒细胞集落刺激因子(G-CSF)对内毒素诱导的急性肺损伤的造血和嗜中性粒细胞活化作用。将豚鼠分为四组:(1)生理盐水对照组,(2)内毒素组,(3)环磷酰胺(CPA)+内毒素组,(4)G-CSF+内毒素组。G-CSF剂量为20 μ g/kg,每天皮下注射两次,持续5天。静脉注射内毒素(0.02和2.0 mg/kg)后观察动物4 h,连续测量全血细胞计数和血流动力学。在死亡时检查肺血管外水、肺组织中的[125 I]白蛋白渗漏和组织病理学特征。单纯内毒素组表现为外周白细胞减少、一过性低血压、肺水过多、白蛋白渗漏增加、肺组织中PMN蓄积和大体组织病理学水肿。与内毒素单独给药组相比,G-CSF给药组动物的外周白细胞减少、肺水过多和白蛋白渗漏反应减弱。在G-CSF组中未观察到增强的反应。CPA+内毒素组肺损伤减轻,与G-CSF组相似。总之,G-CSF预处理倾向于减弱而不是增强嗜中性粒细胞依赖性急性肺内毒素反应。
We studied recombinant human granulocyte colony-stimulating factor (G-CSF) in terms of its hematopoietic and neutrophil-activating effects on acute lung injury induced by endotoxin. Guinea pigs were divided into four groups: (1) saline control animals, (2) endotoxin alone, (3) cyclophosphamide (CPA)+endotoxin, and (4) G-CSF+endotoxin. A G-CSF dose of 20 micrograms/kg was given subcutaneously twice a day for 5 days. Animals were observed for 4 h after intravenously administered endotoxin (0.02 and 2.0 mg/kg) with serial measurements of complete blood counts and hemodynamics. Lung extravascular water, [125I]albumin leakage in lung tissue, and histopathologic features were examined at death. The endotoxin-alone group showed peripheral leukopenia, transient hypotension, excess lung water, increased albumin leakage, PMN accumulation in lung tissue, and gross histopathologic edema. G-CSF-treated animals showed attenuated responses in peripheral leukopenia, excess lung water, and albumin leakage in comparison with the endotoxin-alone group. No augmented responses were seen in the G-CSF group. The CPA+endotoxin group also had attenuated lung injury, which was similar to that in the G-CSF group. In conclusion, pretreatment with G-CSF tended to attenuate rather than enhance neutrophil-dependent acute lung responses to endotoxin.
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