CAJ | 학술논문

目的探讨胆道梗阻型损伤后胆管、肝脏及局部组织的病理变化过程，从中获得最佳手术修复时机的病理学基础。方法运用家犬制作梗阻型胆道损伤动物模型，动态观察胆管梗阻损伤后不同时间段内胆管形态学、局部组织病理学和肝脏病理学指标的变化情况。结果胆管梗阻型损伤后，近端胆管随着压力的增加而持续扩张，第15天达(18.91±1.85)mm。损伤胆管局部组织出现急性炎症反应。损伤早期（10 d之内）管壁炎性细胞浸润增多，黏膜水肿加重，胆管壁呈炎性水肿样增厚。至梗阻后期（15d之后）炎性细胞浸润减少，水肿减轻，黏膜层变薄，成纤维母细胞增生及胶原组织增生广泛，管壁纤维增生性增厚。定量分析炎症水肿程度显示，以5d时最严重（HE染色WBC计数54.2士5.8个），到第15天炎症消退明显(HE染色WBC计数41.7士7.2比54.2±5.8个，P＜0.05)。同时，在梗阻早期（BDL5、BDL10组）肝脏出现轻至中度的肝细胞浊肿变性伴脂肪变性，肝窦扩张充血。随着阻塞时间的延长，至梗阻后期(20 d、30 d)肝细胞出现广泛的空泡变性及肝窦闭塞。结论急性梗阻型胆管损伤后早期(5 d)出现胆管急速扩张，胆管及周围组织炎症水肿，肝实质损害。15d后局部炎症水肿消退，代之纤维及胶原增生。20 d后肝实质出现不可逆损害。综合局部环境及全身条件认为梗阻后10～20 d是手术进行一期修复的最好时间段。
목적 탐토담도경조형손상후담관、간장급국부조직적병리변화과정，종중획득최가수술수복시궤적병이학기출。방법운용가견제작경조형담도손상동물모형，동태관찰담관경조손상후불동시간단내담관형태학、국부조직병이학화간장병이학지표적변화정황。결과 담관경조형손상후，근단담관수착압력적증가이지속확장，제15천체(18.91±1.85)mm。손상담관국부조직출현급성염증반응。손상조기（10 d지내）관벽염성세포침윤증다，점막수종가중，담관벽정염성수종양증후。지경조후기（15d지후）염성세포침윤감소，수종감경，점막층변박，성섬유모세포증생급효원조직증생엄범，관벽섬유증생성증후。정량분석염증수종정도현시，이5d시최엄중（HE염색WBC계수54.2사5.8개），도제15천염증소퇴명현(HE염색WBC계수41.7사7.2비54.2±5.8개，P＜0.05)。동시，재경조조기（BDL5、BDL10조）간장출현경지중도적간세포탁종변성반지방변성，간두확장충혈。수착조새시간적연장，지경조후기(20 d、30 d)간세포출현엄범적공포변성급간두폐새。결론급성경조형담관손상후조기(5 d)출현담관급속확장，담관급주위조직염증수종，간실질손해。15d후국부염증수종소퇴，대지섬유급효원증생。20 d후간실질출현불가역손해。종합국부배경급전신조건인위경조후10～20 d시수술진행일기수복적최호시간단。
Objective To explore the histopathological changes of bile duct,liver and local tissue for injurious biliary stricture(IBS). Method To observe the morphological and pathological changes of bile duct, local tissue and liver in different periods with dogs as the established animal model for IBS. Result Bile duct obstruction due to injury can expand the proximal bile duct up to 18.91 ±1.85 mm as the pressure goes up. Damage to local tissue triggers acute inflammation. In early injury phase (within 10 d), inflammatory cell infiltration and proliferation appears on the wall of the duct with increased mucosal edema as well as thickening of the biliary ductile wall. In the late injury phase (15 d), the degree of infiltration of inflammatory cells, edema and mucosal thickness were reduced whereas fibroblast and collagen tissue were proliferated extensively. The wall of biliary duct also becomes fibrotic and thickens. Quantitative analysis of the inflammatory edema shows the most severe outcome on the 5th day (HE staining WBC count of 54.2±5.8 unit) and its severity progressively subsides on the 15th day. (HE staining WBC count of 41.7±7.2 vs 54.2±5.8 a, P＜0.0,5). In the early obstruction (5 d and 10 d), the liver cells showed mild to moderate swelling and its degeneration is often associated with steatosis and sinusoidal expansion and congestion. As the obstruction time increases in the 20 d and 30 d group, liver cells starts to show extensive vacuolation and sinusoidal occlusion. Conclusions Early phase (5 days) of acute bile duct obstruction due to injury shows rapid expansion of the bile duct, edema in the bile duct itself as well as its surrounding tissue and liver damage. After 15 days, the local inflammatory edema is greatly reduced and is replaced by hyperplasia of fibers and collagen. Liver damage appears to be irreversible after 20 days. Considering local environmental and systemic conditions, the optimal time frame to repair obstruction of bile duct surgically is between 10-20 days.