【作者】 周发春；

【导师】 黄纪坚；

【作者基本信息】 重庆医科大学 ， 急诊医学， 2003， 硕士

【摘要】 目的 通过对大鼠油酸型ARDS模型肺、心、脑的形态学观察，探讨油酸致大鼠ARDS引起的形态学改变的机理，为临床治疗ARDS提供一定的理论依据。方法 采用纯种Wistar大鼠，实验组从舌静脉注入油酸（OA 0.1ml/Kg ，n=10）,对照组（n=5）从舌静脉注入等体积生理盐水。造模2小时后将大鼠快速断颈取大脑皮质、肺组织及右心房肌组织。经光镜和透射电镜观察对照组和实验组三种组织的形态学改变；并测定肺组织的湿干重比和肺系数；采用立体计量法测定肺II型细胞板层小体与细胞质面密度比（%）。结果 1.造模2hr后肺组织内皮细胞通透性增强，超微结构表现为：微吞饮小泡增多，内皮细胞肿胀及凋亡改变；肺上皮细胞（包I、II型细胞）肿胀及板层小体数量减少，空化明显；肺泡腔有大量血浆、纤维素物质及血细胞渗出；肺间质轻度增生及炎症细胞（以中性粒细胞为主）浸润。2.心房肌组织：心肌细胞核轻度溶解，肌丝呈灶性溶解，线粒体轻度内室肿胀，肌浆网轻度扩张；特殊心房颗粒（SAG）减少或消失。内皮细胞核异染色质边集或固缩，胞浆电子密度变深，并有空化。3.大脑组织：少数神经元存在不同程度的肿胀，表现为核轻度溶解及胞浆肿胀，以靠近毛细血管附近的神经元最为明显；毛细血管周围水肿明显，内皮细胞仅表现为微吞饮小泡增多，紧<WP=6>密连接正常。结论 1.油酸致大鼠发生ARDS肺部改变的形态学基础是：油酸直接损伤肺毛细血管内皮及肺泡上皮，导致血管内血浆及血细胞渗出到肺泡腔，并有Ⅱ型细胞内表面活性物质的损耗，肺泡塌陷致肺换气功能障碍，发生进行性低氧血症。2.油酸致大鼠ARDS后2hr，心房肌毛细血管内皮细胞及心肌细胞均表现为缺氧性超微结构改变；这种改变可能与ARDS所致进行性低氧血症有关，同时毛细血管内皮细胞有凋亡改变。3.油酸致大鼠ARDS后2hr，大脑皮层毛细血管内皮细胞神经元胞体和轴浆均出现轻度肿胀溶解性改变。毛细血管周围水分增多。这些改变与ARDS继发性进行性低氧血症有关。更多还原

【Abstract】 Objectives To probes the morphologic changes and its injury mechanism of the lung, heart and brain in the oleic-induced ARDS rats; to provide the theoretic basis for the clinic treatment on ARDS patients. Methods 15 Pure Wistar rats were divided into the experiment and the control group randomly. The amount of 0.1ml/Kg oleic acid were injected through lingua vein in the experiment group (n=10); and the same amount of N.S were injected instead in the control group (n=5). Rats were killed after 2 hours and the cerebral cortex, lung tissue and right atria were obtained. The morphologic changes of these three tissues were observed with light microscope and transmission electronic microscope; the pulmonary wet-to-dry weight ratio, the pulmonary weight indexs, and the ratio of the area of the multilamellar body to the area of cytoplasm in type II alveolar cell were measured.Results 1.The permeability of the pulmonary endothelial cells increased 2 hours after the injection of oleic acid. Ultrastructure revealed increased amount of micropinocytosis vesicles, swelling of endothelial cells and apoptosis; the swelling of pulmonary epithelial (type I and type II), the reduced amount of multilamellar body with significant cavitation; the alveolar cavities were infiltrate with large amount of<WP=8>plasma, fibrin substance and blood cells; mild pulmonary interstitial hyperplasia and infiltration of inflammatory cells (predominantly polymorphonuclear leukocyte). 2. The myocardic cells: slight dissolution of nucleus, dotted dissolve of myofilament, mild swelling of the inner chamber of mitochondria, mildly enlarged saroplasmic reticulun; SAG reduced or disappeared; margination or pycnosis for the heterochromatin of endothelial cells nucleus, heavier change of the electronic density of plasm, with some cavitation.3.The brain tissues: some neurons were swelling in different degree, which displayed to be the mild dissolve of nucleus and swelling of plasma (mostly for the neuron near the capillaries); significant edema at the pericapillaries area, the endothelial cells showed only increased amount of micropinocytosis vesicle, with normal tight junction. Conclusions 　1.The basic morphological changes of the oleic-induced ARDS lungs among rats was that: oleic acid directly injured pulmonary capillary endothelial cells and alveolar epithelium, resulted in the infiltration of plasma and blood cells into the alveolar lumen, led to the reduction of PS in the alveolar type II cells, and cause to the collapse of the alveolar lumen and disability of lung function, and produce progressive hypoxemia.2. The ultrastructure of myocardium capillary endothelial cells and myocardial cells displayed to be an anoxia change 2 hours later after the oleic injection. This change might be related to progressive hypoxemia resulted from ARDS. In addition, as apoptosis of capillary endothelial cells were observed. 3.Neurons and capillary endothelial cells of cerebral cortex were swelling and mildly dissolved 2 hours later after the oleic induced ARDS in rats. At the mean time, there was an increase of water around the<WP=9>capillaries. All of these changes may related to the secondary progressive hypoxemia.更多还原