梗阻性黄疸大鼠应激时胃粘膜微循环变化观察  

Stress induced changes of the gastric mucosal microcirculation in rats with obstructive jaundice

作　　者：段建中[1] 杨乃众[2] 李占文[2] 李晓强 杜如昱[2] 

机构地区：[1]包头医学院第一附属医院普外科,014010 [2]北京医科大学人民医院普外科 [3]华北煤炭部医学院附属医院外科

出　　处：《中华普通外科杂志》1998年第3期160-162,共3页Chinese Journal of General Surgery

摘　　要：目的探讨胃粘膜微循环在梗阻性黄疸应激性溃疡发病机制中的作用。方法用激光多普勒血流仪测定胃粘膜血流,在光镜和电镜下观察胃粘膜微血管形态学和超微结构的变化。结果梗阻性黄疸大鼠冷束缚应激后胃粘膜血流减少,明显低于对照组(P<0.01)。胃粘膜表层和粘膜下层血管明显淤血,微血管通透性增强。结论梗阻性黄疸大鼠应激时胃粘膜血流减少是应激性溃疡发病机制中的重要因素,应激时胃粘膜微血管内皮细胞表面糖蛋白层的损伤可能是导致微血管通透性增强的发病因素之一。Objective The aim of the present study was to observe the role of the gastric mucosal microeirculation in the pathogenesis of the stress ulcer of cold and restraint stress(CRS) on the rat with obstructive jaundice. Method Gastric mucosal blood flow(GMBF)was measured with laser dopple flowmeter,and changes on the gastric microvascular morphology and ultrastruction were investigated with light-and electro-microscopy.Re- sults The experimental results indicated that:GMBF in test groups decreased and is significantly lower than that in control groups (P<0.01) after CRS.Vascular stasis in the surface and submucosal vessels of the rat with obstructive jaundice was observed with light microscopy.The glucoprotein layer in the surface of the mi- crovascular endothelial cells was damaged and microvascular permeability increased.Conclusion CRS de- creases GMBF and vascular stasis is one of the important factors in the pathogenesis of stress ulcer on the rat with obstructive jaundice.Stress induced injury of the glucoprotein layer in the surface of the vascular endothe- lial cells might be one of the factors that cause the increase of the microvascular permeabiliy.LaCl3 was a more sensible tracer in studying the microvascular permeability with electromicroscopy.

关 键 词：梗阻性黄疸 胃粘膜 微循环 应激 大鼠 手术后 

分 类 号：R657.3[医药卫生—外科学] R656.62[医药卫生—临床医学]