血管活性物质在大鼠肝肺综合征发病中的作用  

Role of vascular mediators in the pathogenesis of hepatopulmonary syndrome in rats

作　　者：倪醒之[1] 吴志勇[1] 陈治平[1] 邝耀麟[1] 

机构地区：[1]上海第二医科大学附属仁济医院普外科,200001

出　　处：《中华普通外科杂志》2004年第10期620-623,共4页Chinese Journal of General Surgery

基　　金：上海市科委基金资助 (98ZB14 0 3 0 )

摘　　要：目的　研究血管活性物质在大鼠肝肺综合征发病中的作用。方法　将Sprague Dawley(SD)大鼠分 4组 :肝前型门静脉高压症 (PHPH)、肝内型 (IHPH)门静脉高压症、门腔端侧分流 (PCS)和手术对照组 (SO)。模型制备后两周 ,行动脉血气、肝功能及肝肺病理检查。检测血清和肺组织NO-2 /NO-3 、内皮素 1(ET 1)、胰高糖素 (Glu)、血管活性肠肽 (VIP)浓度。结果　鼠肺泡细胞无变性坏死 ,肺泡形态正常 ,无炎性细胞浸润、间质水肿、纤维增生和透明膜形成。IHPH鼠肺泡毛细血管增生、扩张 ,肺泡间隔增宽、容量减小。PaO2 :IHPH鼠 (73 85± 6 5 1)mmHg较PHPH鼠 (97 39± 1 33)mmHg、PCS(95 2 3± 2 2 2 )mmHg及SO鼠 (99 0 5± 0 75 )mmHg显著下降。肺组织NO-2 /NO-3 含量 :IHPH鼠(19 78± 5 33) μmol/g显著高于PHPH鼠 (13 2 1± 3 99) μmol/g、PCS鼠 (13 89± 3 16 ) μmol/g和SO鼠(8 71± 1 6 8) μmol/g。IHPH鼠ET 1浓度显著低于其他鼠。肺Glu和VIP含量各组间差异无显著性。结论　肺组织中NO合成增加、ET 1减少 ,是引起HPS鼠肺微血管扩张及动脉性低氧血症的重要原因。Objective To study the role of vascular mediators in the pathogenesis of hepatopulmonary syndrome in rats. Methods Male Sprague-Dawley (SD) rats were divided into four groups: SO (surgical control), IHPH (intrahepatic portal hypertension), PHPH (prehepatic) and PCS (portocaval shunt). Two weeks after pathological study, arterial blood gas and the concentrations of NO, glucagon, VIP and ET-1 in plasma and lung were determined. Results Lung structural alteration of rats induced by CCl 4 was of alveolar capillary dilation and angiogenesis, thickened alveolar septa and decreased alveolar capacity. There was no inflammation, edema, fibrosis, alveolar collapse and hyaline membrane formation in lung of all rats. PaO 2 ( mm?Hg)decreased more significantly in IHPH (73.85±6.51) rats than in PHPH (972?9±1.33), PCS (95.23±2.22) and SO rats (99.05±0.75). The level of lung NO of IHPH (19.78±5.33) was significantly increased than those of PHPH (13.21±3.99) and PCS (13.89±3.16) whose level in lung homogenate increased than those of SO (8.71±1.68). There was no difference of Glu and VIP levels in lung among all rats. The level of lung ET-1 in IHPH was significantly decreased than other rats. Conclusion Increased NO levels and decreased ET-1 levels in lung of HPS rats cause alveolar dilation and angiogenesis leading to mismatched ventilation-perfusion, and decrease of PaO 2.

关 键 词：大鼠 血管活性物质 肝肺综合征 鼠肝 肺组织 发病 肺泡 ET-1 鼠肺 VIP 

分 类 号：R575[医药卫生—消化系统] R563[医药卫生—内科学]