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Intraoperative catecholamine release in brain-dead organ donors is not suppressed by administration of fentanyl

Published online by Cambridge University Press:  11 July 2005

R. D. Fitzgerald
Affiliation:
Ludwig Boltzmann Institute for Economics of Medicine in Anaesthesia and Intensive Care, Vienna, Austria
C. Hieber
Affiliation:
University of Vienna, Department of Anaesthesia and General Intensive Care, Vienna, Austria
E. Schweitzer
Affiliation:
Lainz Hospital, Department of Anaesthesia and Intensive Care, Vienna, Austria
A. Luo
Affiliation:
University of Vienna, Department of Anaesthesia and General Intensive Care, Vienna, Austria
W. Oczenski
Affiliation:
Lainz Hospital, Department of Anaesthesia and Intensive Care, Vienna, Austria
F. X. Lackner
Affiliation:
University of Vienna, Department of Anaesthesia and General Intensive Care, Vienna, Austria
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Extract

Summary

Background and objective: Endogenous catecholamines are released in brain-dead organ donors following painful stimulation during retrieval surgery, and might be harmful to harvested organs. Our hypothesis was that inhibition of pain by fentanyl would inhibit such catecholamine release.

Methods: We tested 17 brain-dead organ donors in a randomized, placebo-controlled, double-blinded study. Blood samples for determination of epinephrine and norepinephrine concentrations were obtained before and 10 min after in take of either fentanyl 7 μg kg−1 or an equivalent volume of placebo. Further points of measurement were taken after skin incision and sternotomy. Mean arterial pressure and heart rate at these points were recorded.

Results: Catecholamine concentrations rose following painful stimuli. No differences in haemodynamics, between the fentanyl and the placebo group were detectable. Epinephrine concentrations, but not those of norepinephrine, were higher in the fentanyl group, reaching significance following sternotomy.

Conclusion: We conclude that the use of fentanyl (7 μg kg−1) was not effective in suppressing the catecholamine release, following painful surgical stimulation in brain-dead organ donors.

Type
Original Article
Copyright
© 2003 European Society of Anaesthesiology

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References

Wahlers T, Cremer J, Fieguth, et al. Donor heart-related variables and early mortality after heart transplantation. J Heart Lung Transplant 1991; 10: 2227.Google Scholar
Mackersie RC, Bronsther OL, Shackford SR. Organ procurement in patients with fatal head injuries. Ann Surg 1991; 213: 143150.Google Scholar
Mertes PM, Carteaux JP, Jaboin Y, et al. Estimation of myocardial interstitial norepinephrine release after brain death using cardiac microdialysis. Transplantation 1994; 57: 371377.Google Scholar
Fitzgerald RD, Dechtyar I, Templ E, Fridrich P, Lackner FX. Cardiovascular and catecholamine response during surgery in brain-dead organ donors. Anaesthesia 1995; 50: 388392.Google Scholar
Fitzgerald RD, Dechtyar I, Templ E, Pernerstorfer T, Hackl W, Lackner FX. Endocrine stress reaction in brain dead organ donors. Transpt Intern 1996; 9: 102108.Google Scholar
Depret J, Teboul JL, Benoit G, Mercat A, Richard C. Global energetic failure in brain-dead patients. Transplantation 1995; 60: 966971.Google Scholar
Ghosh S, Bethune DW, Hardy I, Kneeshaw J, Latimer RD, Oduro A. Management of donors for heart and heart–lung transplantation. Anaesthesia 1990; 45: 672675.Google Scholar
Wicomb WN, Cooper DK, Lanza RP, Novitzky D, Isaacs S. The effects of brain-death and 24 hours storage by hypothermic perfusion on donor heart function in the pig. J Cardiovasc Surg 1986; 91: 896909.Google Scholar
Galinanes M, Hearse DJ. Brain-death-induced cardiac contractile dysfunction: studies of possible neurohormonal and blood-borne mediators. J Mol Cell Cardiol 1994; 26: 481498.Google Scholar
White M, Wiechmann RJ, Roden RL, et al. Cardiac beta-adrenergic neuroeffector systems in acute myocardial dysfunction related to brain injury. Evidence for catecholamine-mediated damage. Circulation 1995; 92: 21832189.Google Scholar
Tolksdorf W, Schafer E, Pfeiffer J, Mittelstaedt G. Adrenalin-, Noradrenalin-, Blutdruck und Herzfrequenzverhalten während der Intubation in Abhängigkeit unterschiedlicher Fentanyl-Dosen. Anästh Intensivther Notfallmed 1987; 22: 171176.Google Scholar