HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Eberl, T. Articles by Margreiter, R. Search for Related Content PubMed PubMed Citation Articles by Eberl, T. Articles by Margreiter, R.

Ann Thorac Surg 1996;62:526-532
© 1996 The Society of Thoracic Surgeons

---

Original Articles: Cardiovascular

Assessment of Endothelial Preservation in Human Cell Cultures

Departments of Transplant Surgery, Internal Medicine, and Gynecology and Obstetrics, University Hospital Innsbruck, and Department of Zoology, University of Innsbruck, Innsbruck, Austria

Accepted for publication April 6, 1996.

Background. Impairment of microcirculation due to endothelial cell damage must be considered a limiting factor in organ preservation. The present study aims at a quantitative assessment of preservation-induced injury in cultured human endothelial cells.

Methods. Monolayer cultures of human umbilical vein endothelial cells were exposed to cold (4°C) hypoxic storage in University of Wisconsin solution, histidine-tryptophane-ketoglutarate solution, Euro-Collins solution, and saline solution. Cellular integrity was evaluated by viable cell count, ultrastructural analysis, and prostacyclin release after 24, 48, and 72 hours of storage and subsequent 6 hours of reincubation in culture medium at 37°C. Expression of intercellular adhesion molecule-1 was investigated after 6, 12, and 24 hours of cold preservation and after 6 hours of rewarming.

Results. Cellular viability was best maintained with University of Wisconsin and histidine-tryptophane-ketoglutarate solutions with no significant reduction of cell count up to 72 hours; Euro-Collins solution and saline solution caused a significant decline in cell numbers after 24 hours (p < 0.05). Morphology was best preserved by University of Wisconsin solution. Prostacyclin values were elevated after 24 hours in Euro-Collins solution and saline solution, after 48 hours in histidine-tryptophane-ketoglutarate, Euro-Collins, and saline solutions, and after 72 hours in Euro-Collins solution (p < 0.05, compared with University of Wisconsin solution). ICAM expression was weak after cold storage (24 hours) in University of Wisconsin solution, moderate after incubation in histidine-tryptophane-ketoglutarate and Euro-Collins solutions and intensive after storage in saline solution. In contrast, rewarming caused intensive expression of intercellular adhesion molecule-1 in all experimental groups as compared with controls, which showed baseline expression at any time.

Conclusions. From our results we conclude that in this model cellular integrity is best protected by University of Wisconsin solution, increased prostacyclin release is consistent with morphologic alterations and intercellular adhesion molecule-1 expression is clearly up-regulated in endothelial cells under reperfusion conditions after cold hypoxic storage.

This article has been cited by other articles:

				F. Alamanni, A. Parolari, R. Visigalli, O. Bussolati, P. Rubini, R. Sala, L. Bonati, G. C. Gazzola, P. Biglioli, and V. Dall'Asta Endothelial cell injury induced by preservation solutions: a confocal microscopy study Ann. Thorac. Surg., May 1, 2002; 73(5): 1606 - 1614. [Abstract] [Full Text] [PDF]