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 262: G345-G350, 1992;
0193-1857/92 $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 Lindert, K. A.
Right arrow Articles by Thurman, R. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lindert, K. A.
Right arrow Articles by Thurman, R. G.

AJP - Gastrointestinal and Liver Physiology, Vol 262, Issue 2 345-G350, Copyright © 1992 by American Physiological Society

ARTICLES

Activation of Kupffer cells on reperfusion following hypoxia: particle phagocytosis in a low-flow, reflow model

K. A. Lindert, J. C. Caldwell-Kenkel, S. Nukina, J. J. Lemasters and R. G. Thurman
Department of Pharmacology, University of North Carolina, Chapel Hill 27599.

Hypoxia is produced selectively in pericentral regions of the liver lobule with a low-flow, reflow perfusion model in which the flow rate is reduced to approximately one-third to one-fourth of normal. This model was used to monitor carbon particle phagocytosis by Kupffer cells during hypoxia and reoxygenation. At normal flow rates, oxygen uptake was 131 mumol.g-1.h-1, pressure was 7.5 cmH2O, and carbon uptake was 150 mg.g-1.h-1. During the low-flow period, oxygen uptake, pressure, and carbon uptake decreased to values of 54 mumol.g-1.h-1, 6.4 cmH2O and 83 mg.g-1.h-1, respectively. Upon reflow, oxygen uptake and pressure increased to 141 mumol.g-1.h-1 and 10.3 cmH2O, respectively. In addition, carbon uptake was elevated approximately threefold to 234 mg.g-1.h-1, indicating activation of Kupffer cells. This activation was prevented by pretreatment with methyl palmitate, a known inhibitor of Kupffer cells. Histological examination revealed significantly more Kupffer cells laden with carbon particles in untreated livers after reflow than in livers from methyl palmitate-treated or untreated rats. Electron microscopic analysis of livers at reflow revealed Kupffer cells with numerous pseudopodia and lamellapodia, reflecting an activated state. These changes were absent in controls or in livers perfused under low-flow conditions. This study demonstrates that Kupffer cells are activated on reoxygenation after hypoxia.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
S. L. Lindell, S. L. Klahn, T. M. Piazza, M. J. Mangino, J. R. Torrealba, J. H. Southard, and H. V. Carey
Natural resistance to liver cold ischemia-reperfusion injury associated with the hibernation phenotype
Am J Physiol Gastrointest Liver Physiol, March 1, 2005; 288(3): G473 - G480.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
P. Schemmer, N. Enomoto, B. U. Bradford, H. Bunzendahl, J. A. Raleigh, J. J. Lemasters, and R. G. Thurman
Activated Kupffer cells cause a hypermetabolic state after gentle in situ manipulation of liver in rats
Am J Physiol Gastrointest Liver Physiol, June 1, 2001; 280(6): G1076 - G1082.
[Abstract] [Full Text] [PDF]


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