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本文引用的文献

1
Organ failure associated with severe acute pancreatitis.与重症急性胰腺炎相关的器官衰竭。
World J Gastroenterol. 2003 Nov;9(11):2570-3. doi: 10.3748/wjg.v9.i11.2570.
2
Neutrophils and NADPH oxidase mediate intrapancreatic trypsin activation in murine experimental acute pancreatitis.中性粒细胞和NADPH氧化酶介导小鼠实验性急性胰腺炎胰腺内胰蛋白酶的激活。
Gastroenterology. 2002 Apr;122(4):974-84. doi: 10.1053/gast.2002.32409.
3
Persistent multiple organ microcirculatory disorders in severe acute pancreatitis: experimental findings and clinical implications.重症急性胰腺炎中持续存在的多器官微循环障碍：实验结果与临床意义
Dig Dis Sci. 2002 Jan;47(1):130-8. doi: 10.1023/a:1013284008219.
4
[Apoptosis of endothelial cells in alteration of microvascular permeability in lung during sepsis].[脓毒症时肺微血管通透性改变中内皮细胞的凋亡]
Zhonghua Wai Ke Za Zhi. 2000 May;38(5):385-7.
5
[The feature of pancreatic microcirculatory impairment in caerulein induced acute pancreatitis].[蛙皮素诱导的急性胰腺炎中胰腺微循环障碍的特征]
Zhonghua Wai Ke Za Zhi. 1999 Mar;37(3):138-40, 9.
6
Involvement of soluble adhesion molecules in acute pancreatitis.可溶性黏附分子与急性胰腺炎的关系
Eur Surg Res. 2001 Sep-Dec;33(5-6):377-82. doi: 10.1159/000049733.
7
Endothelial-derived selectins in the development of organ dysfunction in acute pancreatitis.
Crit Care Med. 2001 Mar;29(3):567-72. doi: 10.1097/00003246-200103000-00018.
8
Differential upregulation of cellular adhesion molecules at the sites of oxidative stress in experimental acute pancreatitis.实验性急性胰腺炎氧化应激部位细胞黏附分子的差异性上调
J Surg Res. 2001 Mar;96(1):56-67. doi: 10.1006/jsre.2000.6052.
9
Blocking pulmonary ICAM-1 expression ameliorates lung injury in established diet-induced pancreatitis.阻断肺部ICAM-1表达可改善已建立的饮食诱导性胰腺炎中的肺损伤。
Ann Surg. 2001 Feb;233(2):213-20. doi: 10.1097/00000658-200102000-00010.
10
Neutrophils, not complement, mediate the mortality of experimental hemorrhagic pancreatitis.中性粒细胞而非补体介导实验性出血性胰腺炎的致死率。
Pancreas. 2001 Jan;22(1):40-6. doi: 10.1097/00006676-200101000-00007.

微循环障碍影响急性重症胰腺炎大鼠肺损伤后的情况。

Microcirculation disturbance affects rats with acute severe pancreatitis following lung injury.

作者信息

Liu Xue-Min, Liu Qing-Guang, Xu Jun, Pan Cheng-En

机构信息

Department of Hepatobiliary Surgery, Xi'an Jiaotong University First Hospital, Xi'an 710061, Shaanxi Province, China.

出版信息

World J Gastroenterol. 2005 Oct 21;11(39):6208-11. doi: 10.3748/wjg.v11.i39.6208.

DOI:10.3748/wjg.v11.i39.6208
PMID:16273652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4436642/
Abstract

AIM

To study the effects of microcirculation disturbance (MD) on rats with acute severe pancreatitis (ASP).

METHODS

We developed ASP rat models, and anatomized separately after 1, 3, 5, 7, and 9 h. We took out blood and did hemorrheologic examination and erythrocyte osmotic fragility test, checked up the water content, capillary permeability, and genetic expression of intercellular adhesion molecule-1 (ICAM-1) in lung tissues, examined the apoptosis degree of blood vessel endothelium while we tested related gene expression of Bax and Bcl-2 in lung tissues. We did the same examination in control group.

RESULTS

The viscosity of total blood and plasma, the hematocrit, and the erythrocyte osmotic fragility were all increased. Fibrinogen was decreased. The water content in lung tissues and capillary permeability were increased. Apoptosis degree of blood vessel endothelium was increased too. ICAM-1 genetic expression moved up after 1 h and reached its peak value after 9 h.

CONCLUSION

MD plays an important role in ASP following acute lung injury (ALI). The functional damage of blood vessel endothelium, the apoptosis of capillary vessel endothelium, WBC edging-concentration and the increasing of erythrocyte fragility are the main reasons of ALI.

摘要

目的

研究微循环障碍（MD）对急性重症胰腺炎（ASP）大鼠的影响。

方法

建立ASP大鼠模型，于1、3、5、7和9小时后分别进行解剖。取血进行血液流变学检查和红细胞渗透脆性试验，检测肺组织含水量、毛细血管通透性及细胞间黏附分子-1（ICAM-1）基因表达，检测血管内皮细胞凋亡程度，同时检测肺组织中Bax和Bcl-2相关基因表达。对照组进行同样检查。

结果

全血和血浆黏度、血细胞比容及红细胞渗透脆性均升高。纤维蛋白原降低。肺组织含水量和毛细血管通透性增加。血管内皮细胞凋亡程度也增加。ICAM-1基因表达于1小时后升高，9小时后达峰值。

结论

MD在ASP继发急性肺损伤（ALI）中起重要作用。血管内皮功能损害、毛细血管内皮细胞凋亡、白细胞边集-聚集及红细胞脆性增加是ALI的主要原因。