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The Journal of Thoracic and Cardiovascular Surgery, Vol 102, 515-525, Copyright © 1991 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
NJ Jansen, W van Oeveren, L van den Broek, HM Oudemans-van Straaten, CP Stoutenbeek, MC Joen, KJ Roozendaal, L Eysman and CR Wildevuur
A placebo-controlled double-blind study of patients undergoing
cardiopulmonary bypass was conducted, comparing the effects of
dexamethasone and a placebo on the activation of the plasmatic systems and
blood cells and on the postoperative course after cardiopulmonary bypass.
In the placebo group two patterns of blood activation could be
distinguished. From the start of bypass, blood-material interaction caused
an increase in complement C3a and elastase concentration. After release of
the aortic cross-clamp, a statistically significant increase was observed
in tumor necrosis factor, leukotriene B4, and tissue plasminogen activator
activity (p less than 0.01, p less than 0.05, p less than 0.05,
respectively). Dexamethasone treatment was not able to inhibit complement
activation and elastase release during cardiopulmonary bypass. However,
dexamethasone treatment effectively inhibited the increase in tumor
necrosis factor, leukotriene B4, and tissue plasminogen activator activity
after release of the crossclamp (p less than 0.01 compared with the placebo
group). In the postoperative period the patients in the placebo group had
hyperthermia and hypotension and required considerable intravenous fluid
administration and cardiotonic treatment. The dexamethasone-treated
patients, however, showed normothermia (p less than 0.01), had
significantly higher blood pressures (p less than 0.01) without supportive
treatment, and consequently were in the intensive care unit for a shorter
period of time. We conclude that dexamethasone prevents the hemodynamic
instability after cardiopulmonary bypass and thus improves the
postoperative course by inhibition of the leukocyte and tissue plasminogen
activator activity generated after release of the aortic crossclamp.
ARTICLES
Inhibition by dexamethasone of the reperfusion phenomena in cardiopulmonary bypass
Department of Cardio-Pulmonary Surgery, University Hospital, Groningen, The Netherlands.
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P. D. Cooper Inhibition by dexamethasone of the reperfusion phenomena in cardiopulmonary bypass J. Thorac. Cardiovasc. Surg., February 1, 1994; 107(2): 621 - 621. [Full Text] |
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P. Menasche, S. Haydar, J. Peynet, C. D. Buit, R. Merval, G. Bloch, A. Piwnica, and A. Tedgui A potential mechanism of vasodilation after warm heart surgery: The temperature-dependent release of cytokines J. Thorac. Cardiovasc. Surg., January 1, 1994; 107(1): 293 - 299. [Abstract] [Full Text] |
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