|
|
||||||||
Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107; and Department of Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130
This article examines the evidence for nitric
oxide (NO) as a protective agent in splanchnic
ischemia-reperfusion and other forms of acute intestinal
inflammation. Four major points emerge from this body of data. First,
acute intestinal inflammation results in an early (i.e., <5 min) and
severe decrease in endothelium-derived NO. Thus the early trigger event
in this condition is a functional loss of NO. Second, administration of
exogenous NO, NO donors, or NO precursors ameliorate splanchnic
ischemia-reperfusion and other forms of acute intestinal
inflammation (i.e., splanchnic trauma). These beneficial effects occur
at physiological levels of NO when given early in the course of the
inflammatory state. Third, blockade of nitric oxide synthase (NOS) or
gene deletion of NOS exacerbates intestinal inflammation. Fourth, there
are a variety of signaling mechanisms that may mediate the protective effect of NO.
synthase blockers; nitric oxide donors; nitric oxide synthase gene-targeted mice; L-arginine
This article has been cited by other articles:
![]() |
S. H. Lee, C. Culberson, K. Korneszczuk, and M. G. Clemens Differential mechanisms of hepatic vascular dysregulation with mild vs. moderate ischemia-reperfusion Am J Physiol Gastrointest Liver Physiol, May 1, 2008; 294(5): G1219 - G1226. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. D. Linehan, G. Kolios, V. Valatas, D. A. F. Robertson, and J. Westwick Effect of corticosteroids on nitric oxide production in inflammatory bowel disease: are leukocytes the site of action? Am J Physiol Gastrointest Liver Physiol, February 1, 2005; 288(2): G261 - G267. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Rickard and J. McHowat Phospholipid metabolite production in human urothelial cells after protease-activated receptor cleavage Am J Physiol Renal Physiol, November 1, 2002; 283(5): F944 - F951. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Booth, T. J. Stalker, A. M. Lefer, and R. Scalia Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo Diabetes, May 1, 2002; 51(5): 1556 - 1564. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Harada, K. P. Pavlick, I. N. Hines, J. M. Hoffman, S. Bharwani, L. Gray, R. E. Wolf, and M. B. Grisham Genome and Hormones: Gender Differences in Physiology: Selected Contribution: Effects of gender on reduced-size liver ischemia and reperfusion injury J Appl Physiol, December 1, 2001; 91(6): 2816 - 2822. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Kankuri, K. Vaali, R. G. Knowles, M. Lahde, R. Korpela, H. Vapaatalo, and E. Moilanen Suppression of Acute Experimental Colitis by a Highly Selective Inducible Nitric-Oxide Synthase Inhibitor, N-[3-(Aminomethyl)benzyl]acetamidine J. Pharmacol. Exp. Ther., September 1, 2001; 298(3): 1128 - 1132. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Booth, T. J. Stalker, A. M. Lefer, and R. Scalia Elevated ambient glucose induces acute inflammatory events in the microvasculature: effects of insulin Am J Physiol Endocrinol Metab, June 1, 2001; 280(6): E848 - E856. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |