This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Doukas, J. Articles by Maino, G. Search for Related Content PubMed PubMed Citation Articles by Doukas, J. Articles by Maino, G.

American Journal of Pathology, Vol 145, 211-219, Copyright © 1994 by American Society for Investigative Pathology

REGULAR ARTICLES

Reversible endothelial cell relaxation induced by oxygen and glucose deprivation. A model of ischemia in vitro

J Doukas, AH Cutler, CA Boswell, I Joris and G Maino
Department of Pathology, University of Massachusetts Medical Center, Worcester 01655.

Endothelial cells (EC) cultured on polymerized silicone deform the underlying substrate, producing microscopically visible wrinkles. This has been interpreted as cellular contraction, and we have previously concluded that EC normally maintain an active contractile tone. Since in ischemic tissues capillaries become "paralyzed" and lose their tone, we decided to examine the effects of glucose and/or oxygen deprivation on EC contractility. Contracting cultures with wrinkled silicone substrates were exposed to complete anoxia with or without exogenous glucose and followed by time-lapse photography. Under either glucose-or oxygen-free conditions, contraction was maintained for up to 4 days. If, however, both oxygen and glucose were removed, cellular contraction was reversed. After a period of 2 to 4 hours substrate wrinkles gradually disappeared, until by 3 to 7 hours, few to no wrinkles remained. Furthermore, within 10 minutes of restoration to normal oxygen (but not glucose) levels, substrate wrinkling reappeared. F- actin microfilament patterns and cell number per unit area were also altered by glucose and oxygen deprivation. Similar results were obtained using large or small vessel EC. We conclude that in the absence of glucose and oxygen EC lose their contractile tone, and that tone can be re-established upon re-exposure to oxygen. These findings should have implications for the pathogenesis of capillary paralysis in ischemia.

This article has been cited by other articles:

				X.W Hu, A Levy, E.J Hart, L.A Nolan, G.R Dalton, and A.J Levi Intra-uterine growth retardation results in increased cardiac arrhythmias and raised diastolic blood pressure in adult rats Cardiovasc Res, November 1, 2000; 48(2): 233 - 243. [Abstract] [Full Text] [PDF]

				M. J. Cipolla, N. Lessov, W. M. Clark, and E. C. Haley Jr Postischemic Attenuation of Cerebral Artery Reactivity Is Increased in the Presence of Tissue Plasminogen Activator • Editorial Comment Stroke, April 1, 2000; 31(4): 940 - 945. [Abstract] [Full Text] [PDF]

				P. J. Chai, J. A. Williamson, A. J. Lodge, C. W. Daggett, J. E. Scarborough, J. N. Meliones, I. M. Cheifetz, J. J. Jaggers, and R. M. Ungerleider Effects of ischemia on pulmonary dysfunction after cardiopulmonary bypass Ann. Thorac. Surg., March 1, 1999; 67(3): 731 - 735. [Abstract] [Full Text] [PDF]

				G. Majno Chronic Inflammation : Links with Angiogenesis and Wound Healing Am. J. Pathol., October 1, 1998; 153(4): 1035 - 1039. [Full Text] [PDF]

				A. Serraf, M. Robotin, N. Bonnet, H. Detruit, B. Baudet, M. G. Mazmanian, P. Herve, and C. Planche ALTERATION OF THE NEONATAL PULMONARY PHYSIOLOGY AFTER TOTAL CARDIOPULMONARY BYPASS J. Thorac. Cardiovasc. Surg., December 1, 1997; 114(6): 1061 - 1069. [Abstract] [Full Text]