Does microcirculation play a role in the pathogenesis of inflammatory bowel diseases? Answers from intravital microscopic studies in animal models

被引:38
作者
Foitzik, T [1 ]
Kruschewski, M [1 ]
Kroesen, A [1 ]
Buhr, HJ [1 ]
机构
[1] Free Univ Berlin, Dept Surg, Benjamin Franklin Med Ctr, D-12200 Berlin, Germany
关键词
inflammatory bowel disease; animal model; microcirculation; intravital microscopy; intestinal barrier; gut permeability;
D O I
10.1007/s003840050179
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
The potential role of intestinal microcirculation for the development of inflammatory bowel diseases (IBD) has not been systematically investigated, mainly because of methodological problems. Using a well-established rodent model of IBD and intravital microscopy, the present study investigated whether (and when) gut microcirculation is disturbed in IBD, and whether microcirculatory disorders contribute to histological and functional alterations in the development of IBD. Colitis was induced by rectal injection of trinitrobenzene sulfonic acid. After 1, 3, and 15 days rats were laparotomized for intravital microscopic determination of mucosal colonic blood flow. In a second series it was examined whether enhancing colonic capillary blood flow by hemodilution therapy stabilizes colonic wall resistance and other electrophysiological parameters of gut permeability. Additional measurements involved hemodynamic monitoring and histological examinations. Colonic capillary blood flow was significantly decreased 3 days after colitis induction (1.8+/-0.05 vs. 2.6+/-0.04 nl/min in healthy control animals) when histology revealed signs of acute inflammation, and normal values after 15 days (2.4+/-0.06 nl/min) when chronic histological changes were evident. Hemodilution therapy enhanced colonic capillary blood flow in the initial stage (2.1+/-0.02 vs. 1.6+/-0.02 nl/min in saline-treated animals with trinitrobenzene sulfonic acid colitis) and improved gut resistance and electronic chlorid secretion (73+/-15 vs. 33+/-8 mu A cm(2)). Histological alterations were not significantly attenuated. Impaired colonic capillary blood flow in the initial stage of experimental colitis and improved mucosal microcirculation with stabilized gut permeability suggests that the early microcirculatory disturbances precede chronic histological changes and influence functional alterations in the course of the disease. Research should be continued in this field because important mechanisms in the pathogenesis of IBD and potentially therapeutic (vasoactive) substances may otherwise be overlooked.
引用
收藏
页码:29 / 34
页数:6
相关论文
共 38 条
[1]   COMPARATIVE RADIOGRAPHIC AND PATHOLOGICAL STUDY OF INTESTINAL VASO-ARCHITECTURE IN CROHNS DISEASE AND IN ULCERATIVE COLITIS [J].
BRAHME, F ;
LINDSTROM, C .
GUT, 1970, 11 (11) :928-+
[2]  
BUCKELL NA, 1980, GASTROENTEROLOGY, V79, P19
[3]   MICROVASCULAR STUDIES IN NONSPECIFIC INFLAMMATORY BOWEL-DISEASE [J].
CARR, ND ;
PULLAN, BR ;
SCHOFIELD, PF .
GUT, 1986, 27 (05) :542-549
[4]   Gastric intramucosal acidosis in mechanically ventilated patients:: Role of mucosal blood flow [J].
Elizalde, JI ;
Hernández, C ;
Llach, J ;
Montón, C ;
Bordas, JM ;
Piqué, JM ;
Torres, A .
CRITICAL CARE MEDICINE, 1998, 26 (05) :827-832
[5]   EXPERIMENTAL-MODELS OF INFLAMMATORY BOWEL-DISEASE [J].
ELSON, CO ;
SARTOR, RB ;
TENNYSON, GS ;
RIDDELL, RH .
GASTROENTEROLOGY, 1995, 109 (04) :1344-1367
[6]   Inflammatory bowel disease: Etiology and pathogenesis [J].
Fiocchi, C .
GASTROENTEROLOGY, 1998, 115 (01) :182-205
[7]   Influence of changes in pancreatic tissue morphology and capillary blood flow on antibiotic tissue concentrations in the pancreas during the progression of acute pancreatitis [J].
Foitzik, T ;
Hotz, HG ;
Kinzig, M ;
Sorgel, F ;
Buhr, HJ .
GUT, 1997, 40 (04) :526-530
[8]   Improvement of pancreatic capillary blood flow does not augment the pancreatic tissue concentration of imipenem in acute experimental pancreatitis [J].
Foitzik, T ;
Hotz, HG ;
Kinzig, M ;
Sorgel, F ;
Klar, E ;
Warshaw, AL ;
Buhr, HJ .
EUROPEAN SURGICAL RESEARCH, 1996, 28 (06) :395-401
[9]  
Foitzik T, 1997, J Gastrointest Surg, V1, P40
[10]  
Fries W, 1998, ALIMENT PHARM THERAP, V12, P229