实验性急性出血坏死性胰腺炎早期肺损伤的超微病理学研究

Ultrastructural pathological study of lung injury in the early stage of experimental acute hemorrhagic and necrotic pancreatitis

目的:通过观察实验性急性出血坏死性胰腺炎(AHNP)早期肺组织的超微病理变化,探讨AHNP肺损伤的发生机制。方法:雄性大鼠,胰胆管内逆行注射5.0%Na-Tc溶液,建立AHNP模型,随机分为3组(给药后30 min、3h、6 h),光镜和电镜下观察AHNP早期肺组织的病理变化。结果:光镜下,实验大鼠胰胆管内注射Na-Tc后30 min出现肺水肿、炎细胞浸润及局灶性肺不张;给药后3 h肺小血管管腔内有血栓形成;给药后6 h可见大片肺不张及炎细胞浸润增多。电镜下,给药后30 min可见肺泡毛细血管内皮细胞线粒体肿胀,管腔内红细胞瘀滞,以及Ⅱ型肺泡上皮细胞板层小体排空和肺泡腔显著狭窄;给药后3 h肺泡毛细血管内皮细胞线粒体严重肿胀,管腔内可见微血栓形成;给药后6 h肺泡腔内可见红细胞和肺泡巨噬细胞,Ⅱ型肺泡上皮细胞板层小体排空明显增多。结论:AHNP实验大鼠肺泡毛细血管内皮细胞广泛受损并诱发血管内微血栓形成是导致肺微循环障碍、引起早期肺损伤的重要原因。

Objective： To observe the ultrastructural pathological changes of lung in the early stage of experimental acute hemorrhagic and necrotic pancreatitis（AHNP） and explore the mechanism of lung injury in AHNP.Methods： AHNP was induced in male rats by intraductal administration of 5.0% sodium taurocholate.Animals were randomly divided into three groups（30 min,3 h and 6 h after administration）.The pathological changes of lung were observed under light and electron microscope in the early stage of AHNP.Results： Under light microscope,the lung edema,inflammatory cell infiltration and focal atelectasis were observed in experimental rats 30 min after administration.Thrombosis was found in small vessels of the lung 3 h after administration.Large area of atelectasis and inflammatory cell infiltration appeared in lung 6 h after administration.Under electron microscope,the mitochondria of endothelial cells of pulmonary alveolar capillary swelled.Accompanied with stasis of red cells in the capillary lumen and the evacuation of lamellar bodies in type Ⅱ alveolar epithelial cells appeared 30 min after administration.The mitochondria of endothelial cells swelled seriously and the microthrombus in the lumen of capillaries of pulmonary alveolus were found 3 h after administration.Some red blood cells and alveolar macrophages in the alveolar space were observed and the evacuation of lamellar bodies significantly increased in type Ⅱ alveolar epithelial cell 6 h after administration.Conclusion： The extensive damage of pulmonary alveolar capillary endothelial cells with the intravascular thrombogenesis in the lung of experimental rats is the main cause of microcirculatory dysfunction of the lung in the early stage of AHNP.