Division of Cardiovascular Medicine (O. A. Hatoum, D. D. Gutterman). Division of Gastroenterology and Hepatology (D. G. Binion), Department of Medicine (O. A. Hatoum, D. G. Binion, D. D. Gutterman), Cardiovascular Research Center (O. A. Hatoum, D. D. Gutterman), Digestive Disease Center (D. G. Binion), Froedtert Memorial Lutheran (D. G. Binion) Hospital, Medical College of Wisconsin (O. A. Hatoum, D. G. Binion, D. D. Gutterman), Milwaukee, WI.
Paradox of simultaneous intestinal ischaemia and hyperaemia in inflammatory bowel disease
Version of Record online: 22 SEP 2005
European Journal of Clinical Investigation
Volume 35, Issue 10, pages 599–609, October 2005
How to Cite
Hatoum, O. A., Binion, D. G. and Gutterman, D. D. (2005), Paradox of simultaneous intestinal ischaemia and hyperaemia in inflammatory bowel disease. European Journal of Clinical Investigation, 35: 599–609. doi: 10.1111/j.1365-2362.2005.01567.x
- Issue online: 22 SEP 2005
- Version of Record online: 22 SEP 2005
- Received 23 August 2005; accepted 27 August 2005
- Crohn's disease;
- inflammatory bowel disease;
- ulcerative colitis;
This review has focused on evidence regarding intestinal perfusion of inflammatory bowel disease (IBD). Basic investigation has defined an altered microvascular anatomy in the affected IBD bowel, which corresponds with diminished mucosal perfusion in the setting of chronic, long-standing inflammation. Diminished perfusion is linked to impaired wound healing, and may contribute to the continued refractory mucosal damage, which characterizes IBD. Alterations in vascular anatomy and physiology in IBD suggests additional possible mechanisms by which micro-vessels may contribute to the initiation and perpetuation of IBD. This begs the following questions: will angiogenesis within the gut lead to sustained inflammation, does the growing vasculature generate factors that transform the surrounding tissue and does angiogenesis generate vascular anastomosis within the gut, with shunting of blood away from the mucosal surface, impairment of metabolism and potentiation of gut damage? Further studies are required to define the mechanisms that underlie the vascular dysfunction and its role in pathophysiology of IBD.