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CARDIOVASCULAR ANESTHESIOLOGY

Perfluorocarbon Administration During Cardiopulmonary Bypass in Rats: An Inflammatory Link to Adverse Outcome?

Fellery de Lange, MD^*, Kenji Yoshitani, MD^*, Alan D. Proia, MD, PhD, G. Burkhard Mackensen, MD, PhD^*, and Hilary P. Grocott, MD, FRCPC^*

From the *Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina; Department of Perioperative Care and Emergency Medicine, University Medical Center Utrecht, Utrecht, The Netherlands; and Department of Pathology, Duke University Medical Center, Durham, North Carolina.

Address correspondence and reprint requests to Fellery de Lange, MD, Department of Perioperative Care and Emergency Medicine, University Medical Center Utrecht, mail stop Q04-2-313, P.O. Box 85500, 3508 GA Utrecht, The Netherlands. Address e-mail to f.delange{at}umcutrecht.nl.

Abstract

BACKGROUND: Perfluorocarbon (PFC) emulsions are artificial oxygen carriers that have been shown to attenuate the effects of air embolism. Cerebral air embolism, known to occur during cardiopulmonary bypass (CPB), may contribute to adverse cerebral outcomes after cardiac surgery. We designed this study to evaluate the effect of a 60% PFC emulsion (perfluoro-tert-butylcyclohexane; PTBCH) on the inflammatory response and neurocognitive outcome of rats after CPB.

METHODS: Twenty-eight Sprague Dawley rats subjected to 60 min of CPB were randomly divided into two groups: PTBCH CPB animals receiving 3 mL/kg of PTBCH into the venous reservoir and control CPB animals receiving 3 mL/kg of 0.9% saline. At several time points, the cytokines interleukin (IL)-1β, IL-6, IL-10, and tumor necrosis factor (TNF)- were measured. Neurocognitive testing was planned postoperatively using the Morris water maze. Histologic samples were obtained in a separate series of experiments.

RESULTS: Physiologic variables were comparable between groups, but the PTBCH CPB animals required more phenylephrine compared with the controls. Cytokine levels in the PTBCH CPB group were significantly higher than in the control group at 2 and 4 h after CPB (P < 0.05). Neurocognitive outcome could not be evaluated as none of the animals in the PTBCH CPB group survived. Myocardial histological analysis revealed increased areas of contraction band necrosis in the PTBCH CPB animals (P = 0.034).

CONCLUSIONS: Administration of PTBCH during CPB was associated with an excessive release of cytokines. This enhanced inflammatory response with subsequent hypotension may have contributed to mortality in rats receiving PTBCH. The observed patterns of myocardial injury indicate global hypoperfusion and catecholamine excess.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999