期刊
CRITICAL CARE
卷 9, 期 1, 页码 R1-R8出版社
BIOMED CENTRAL LTD
DOI: 10.1186/cc2992
关键词
acute lung injury; acute respiratory distress syndrome; neutrophils; T cells; warm pulmonary ischemia-reperfusion injury
Introduction Beside lung transplantation, cardiopulmonary bypass, isolated lung perfusion and sleeve resection result in serious pulmonary ischemia - reperfusion injury, clinically known as acute respiratory distress syndrome. Very little is known about cells infiltrating the lung during ischemia - reperfusion. Therefore, a model of warm ischemia - reperfusion injury was applied to differentiate cellular infiltrates and to quantify tissue damage. Methods Fifty rats were randomized into eight groups. Five groups underwent warm ischemia for 60 min followed by 30 min and 1 - 4 hours of warm reperfusion. An additional group was flushed with the use of isolated lung perfusion after 4 hours of reperfusion. One of two sham groups was also flushed. Neutrophils and oedema were investigated by using samples processed with hematoxylin/eosin stain at a magnification of x 500. Immunohistochemistry with antibody ED-1 ( magnification x 250) and antibody 1F4 ( magnification x 400) was applied to visualize macrophages and T cells. TdT-mediated dUTP nick end labelling was used for detecting apoptosis. Statistical significance was accepted at P < 0.05. Results Neutrophils were increased after 30 min until 4 hours of reperfusion as well as after flushing. A doubling in number of macrophages and a fourfold increase in T cells were observed after 30 min until 1 and 2 hours of reperfusion, respectively. Apoptosis with significant oedema in the absence of necrosis was seen after 30 min to 4 hours of reperfusion. Conclusions After warm ischemia - reperfusion a significant increase in infiltration of neutrophils, T cells and macrophages was observed. This study showed apoptosis with serious oedema in the absence of necrosis after all periods of reperfusion.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据