首页 | 本学科首页   官方微博 | 高级检索  
检索        

门静脉压升高是胆盐诱发急性胰腺炎微循环障碍的始动环节
引用本文:陈友岱,陈槐卿,唐耘熳,涂秋芬,葛冬霞,余昶,江从勋,廖诗平,王蓉.门静脉压升高是胆盐诱发急性胰腺炎微循环障碍的始动环节[J].生物医学工程学杂志,2007,24(6):1280-1285.
作者姓名:陈友岱  陈槐卿  唐耘熳  涂秋芬  葛冬霞  余昶  江从勋  廖诗平  王蓉
作者单位:1. 四川大学,华西基础医学与法医学院,生物医学工程研究室,成都,610041
2. 四川大学,华西基础医学与法医学院,机能实验室,成都,610041
摘    要:有报道,在胆盐诱发的急性胰腺炎早期,胰腺动脉收缩导致了胰腺微循环障碍。本实验的目的就是验证上述发现是否正确。胆胰管内注射牛黄脱氧胆酸钠诱发大鼠和犬胰腺炎;使用活体显微镜观察大鼠胰腺微动脉管径的变化;记录犬胰腺小动脉压的变化;计数机能毛细血管并乘以胰腺湿重校正;用激光多普勒测量胰腺灌流量。我们发现,在诱发胰腺炎后20min内大鼠胰腺微动脉扩张;犬胰腺动脉压从104.5±4.8mmHg降到54.6±5.6mmHg;5min时下腔静脉血的血细胞压积显著低于门静脉血;校正了的胰腺机能毛细血管密度增加。胰腺微循环障碍与门静脉压升高(最多升高9.18±0.78mmHg)同时发生。将门静脉压降低至基础水平可使胰腺灌流量增加约2.4倍。实验显示,在胆盐诱发急性胰腺炎的早期,胰腺动脉发生了扩张而不是收缩;这时门静脉压升高;门静脉压升高大大减小了胰腺血管压差,并导致血浆丢失和局部血液浓缩,导致胰腺微循环障碍。

关 键 词:急性胰腺炎  胆源性胰腺炎  门静脉压  胰腺动脉压  血管扩张  血管收缩  血液浓缩
收稿时间:2007-02-12
修稿时间:2007-05-30

A Sharp Rise in Portal Vein Pressure, not Arterial Constriction,Initiates Bile Salt-induced Pancreatic Microcirculatory Disturbance
Chen Youdai,Chen Huaiqing,Tang Yunman,Tu Qiufen,Ge Dongxia,Yu Chang,Jiang Congxun,Liao Shiping,Wang Ron.A Sharp Rise in Portal Vein Pressure, not Arterial Constriction,Initiates Bile Salt-induced Pancreatic Microcirculatory Disturbance[J].Journal of Biomedical Engineering,2007,24(6):1280-1285.
Authors:Chen Youdai  Chen Huaiqing  Tang Yunman  Tu Qiufen  Ge Dongxia  Yu Chang  Jiang Congxun  Liao Shiping  Wang Ron
Institution:Institute of Biomedical Engineering, Basic Medicine and Forensic Medicine College, Sichuan University, Chengdu 610041, China.
Abstract:It was reported that pancreatic arteries constricted during the early phase of bile salt-induced acute pancreatitis (AP), leading to pancreatic microcirculatory disturbance. We conducted this experiment to verify whether the above-mentioned finding was true. AP was induced with intraductal injection of taurodeoxyholate. Small pancreatic artery pressure in dogs was recorded. Functional capillaries were counted and calibrated by multiplying wet weight of pancreas. Pancreatic perfusion was measured with Laser Doppler flowmeter. Pancreatic arterioles of rats dilated during the initial 20 min of AP, and pancreatic arterial pressure declined during the early phase of AP in dogs (from 104.5 +/- 4.8 mmHg to 54.6 +/- 5.6 mmHg). The hematocrit of blood from inferior vena cava was significantly lower than that of portal vein at 5 min after pancreatitis induction. The "true" pancreatic functional capillary density increased. The early pancreatic microcirculatory disturbance coincided with a marked increase of portal vein pressure (PVP) as high as 9.18 +/- 0.78 mmHg. Reduction of PVP to baseline level was followed by a marked increase of pancreatic perfusion (by 1.4-fold). Arterial dilatation, but not constriction, occurred during the early phase of bile salt-induced AP. The pancreatic microcirculatory disturbance was due to a marked rise in PVP that greatly reduced the pressure difference in the pancreatic blood vessels and increased plasma extravasation which led. to local hemoconcentration.
Keywords:Acute pancreatitis Biliary pancreatitis Portal vein pressure Pancreatic artery pressure Vasodilatation Vasoconstriction Hemoconcentration
本文献已被 CNKI 万方数据 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号