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作 者:汪盛贤 陈意生[1,2] 陈志远[1,2] 谯怡然 郭德玉
机构地区:[1]第三军医大学基础部病理学教研室 [2]成都军区总医院病理科
出 处:《第三军医大学学报》1996年第5期397-400,共4页Journal of Third Military Medical University
摘 要:应用光镜、电镜、图像分析仪观测了大鼠注射内毒素(L组)和氮芥+内毒素(NL组)后1、3、5、12、24、48、72h7个时相点的肺脏病理变化。发现L组肺组织充血、出血、水肿、肺萎陷;毛细血管内大量中性粒细胞(PMN)和血小板滞留、嵌塞、崩解脱粒,内皮细胞肿胀、坏死;肺泡上皮退变,继而Ⅱ型肺泡上皮细胞增生等。病变过程表现为循环障碍、变性坏死和损伤修复3个阶段。先注射氮芥使大鼠外周血PMN减少,再注射内毒素,发现肺脏病变延迟发生,且程度较L组明显减轻。The pulmonary pathological changes in rats in the 1 h, 3 h, 5 h, 12 h, 24 h, 48 h and 72 h after the injection of lipopolysaccharide (LPS, group L) or nitrogen mustard and LPS (group NL) were observed with optical microscope, electron microscope and image analysis. The pathological changes in the lungs in group L were as follows: (1) Congestion, hemorrhage, edema and atelectasis of the pulmonary tissue; (2) Accumulation and degranulation of polymorphonuclear neutrophils (PMN) and platelets; (3) Swelling and necrosis of endothelial cells; (4) Degeneration of alveolar epithelial cells and the subsequent proliferation of type Ⅱ alveolar epithelial cells . These changes could be divided into circulatory disturbance phase, degeneration necrosis phase and injury repairing phase. The pulmonary pathological changes occurred more slowly and less severely in group NL than those in group L. Our findings suggest that PMN plays an important role in the process of pulmonary injury induced with LPS.
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