AJP - GI Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 250: G749-G753, 1986;
0193-1857/86 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Parks, D. A.
Right arrow Articles by Granger, D. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Parks, D. A.
Right arrow Articles by Granger, D. N.

AJP - Gastrointestinal and Liver Physiology, Vol 250, Issue 6 749-G753, Copyright © 1986 by American Physiological Society

ARTICLES

Contributions of ischemia and reperfusion to mucosal lesion formation

D. A. Parks and D. N. Granger

Two theories have been proposed to account for the mucosal injury associated with intestinal ischemia, hypoxia-countercurrent exchange, and oxygen free radicals. The countercurrent mechanism suggests that mucosal injury should occur predominately during the ischemic period, whereas the oxygen free radical hypothesis predicts that the majority of mucosal injury results from reperfusion of ischemic tissue. Histological specimens obtained during the ischemic period and following reperfusion allowed a systematic evaluation of the time course of development of mucosal lesions in a regional ischemia model. Reperfusion after 3 h of regional hypotension reduced mean mucosal thickness from 1,022.2 +/- 6.3 to 503.6 +/- 10.0 microns. The decrease in mucosal thickness was largely due to a reduction in villus height, inasmuch as the reduction in crypt depth was statistically insignificant. A significantly smaller change in mucosal thickness was observed when the bowel was subjected to 3 h ischemia without reperfusion. The mucosal injury produced by 3 h ischemia and 1 h reperfusion was more severe than that produced by 4 h ischemia without reperfusion. The results of this study suggest that most of the tissue damage produced by the widely employed regional hypotension model occurs at the time of reperfusion.


This article has been cited by other articles:


Home page
 Physiol. Rev.Home page
A. T. Blikslager, A. J. Moeser, J. L. Gookin, S. L. Jones, and J. Odle
Restoration of Barrier Function in Injured Intestinal Mucosa
Physiol Rev, April 1, 2007; 87(2): 545 - 564.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
H. Tsuboi, Y. Naito, K. Katada, T. Takagi, O. Handa, S. Kokura, H. Ichikawa, N. Yoshida, M. Tsukada, and T. Yoshikawa
Role of the thrombin/protease-activated receptor 1 pathway in intestinal ischemia-reperfusion injury in rats
Am J Physiol Gastrointest Liver Physiol, February 1, 2007; 292(2): G678 - G683.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
T. Fujise, R. Iwakiri, B. Wu, S. Amemori, T. Kakimoto, F. Yokoyama, Y. Sakata, S. Tsunada, and K. Fujimoto
Apoptotic pathway in the rat small intestinal mucosa is different between fasting and ischemia-reperfusion
Am J Physiol Gastrointest Liver Physiol, July 1, 2006; 291(1): G110 - G116.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online