| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
INFLAMMATION/IMMUNITY/MEDIATORS
1Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana; and 2Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan
Submitted 31 May 2005 ; accepted in final form 3 August 2005
Human inflammatory bowel diseases (IBD) are associated with significant alterations in intestinal blood flow, the direction and magnitude of which change with disease progression. The objectives of this study were to determine the time course of changes in colonic blood perfusion that occur during the development of dextran-sodium-sulfate (DSS)-induced colonic inflammation and to address the mechanisms that may underlie these changes in blood flow. Intravital microscopy was used to quantify blood flow (from measurements of vessel diameter and red blood cell velocity) in different-sized submucosal arterioles of control and inflamed colons in wild-type (WT) mice. A significant (18–30%) reduction in blood flow was noted in the smallest arterioles (<40 µm diameter) on days 4–6 of DSS colitis. The arteriolar responses to bradykinin in control and DSS-treated WT mice revealed an impaired endothelium-dependent, but not endothelium-independent, vasodilation in the inflamed colon. However, this impaired vasodilatory response to bradykinin after DSS treatment was not evident in mutant mice that overexpress Cu,Zn-superoxide dismutase. Rescue of the bradykinin-induced vasodilation during DSS colitis was also observed in mice that are genetically deficient in the NAD(P)H oxidase subunit gp91phox. These findings indicate that the decline in blood flow during experimental colitis may result from a diminished capacity of colonic arterioles to respond to endogenous endothelium-dependent vasodilators like bradykinin and that NAD(P)H oxidase-derived superoxide plays a major role in the induction of the inflammation-induced endothelium-dependent arteriolar dysfunction.
arterioles; endothelium-dependent vasodilation; colon; superoxide; NAD(P)H oxidase
This article has been cited by other articles:
|
|
 |
|
  L. Deban, C. Correale, S. Vetrano, A. Malesci, and S. Danese Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades Am. J. Pathol., June 1, 2008; 172(6): 1457 - 1466. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Petersson, O. Schreiber, A. Steege, A. Patzak, A. Hellsten, M. Phillipson, and L. Holm eNOS involved in colitis-induced mucosal blood flow increase Am J Physiol Gastrointest Liver Physiol, December 1, 2007; 293(6): G1281 - G1287. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. E. Lomax, M. O'Reilly, S. Neshat, and S. J. Vanner Sympathetic vasoconstrictor regulation of mouse colonic submucosal arterioles is altered in experimental colitis J. Physiol., September 1, 2007; 583(2): 719 - 730. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Horowitz, D. G. Binion, V. M. Nelson, Y. Kanaa, P. Javadi, Z. Lazarova, C. Andrekopoulos, B. Kalyanaraman, M. F. Otterson, and P. Rafiee Increased arginase activity and endothelial dysfunction in human inflammatory bowel disease Am J Physiol Gastrointest Liver Physiol, May 1, 2007; 292(5): G1323 - G1336. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J Ravnic, M. A Konerding, A. Tsuda, H. T Huss, T. Wolloscheck, J. P Pratt, and S. J Mentzer Structural adaptations in the murine colon microcirculation associated with hapten-induced inflammation Gut, April 1, 2007; 56(4): 518 - 523. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
