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Am J Physiol Gastrointest Liver Physiol (August 4, 2005). doi:10.1152/ajpgi.00247.2005
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Submitted on May 31, 2005
Accepted on August 3, 2005

COLONIC BLOOD FLOW RESPONSES IN EXPERIMENTAL COLITIS: TIME-COURSE AND UNDERLYING MECHANISMS

Mikiji Mori1, Karen Y. Stokes1, Thorsten Vowinkel1, Naoyuki Watanabe1, John W. Elrod1, Norman R. Harris1, David J. Lefer1, Toshifumi Hibi2, and D. Neil Granger1*

1 Department of Molecular and Cellular and Physiology, LSU Health Sciences Center, Shreveport, LA, USA
2 Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: dgrang{at}lsuhsc.edu.

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 colon 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 following DSS treatment was not evident in mutant mice that overexpress CuZn-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.




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