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Ann Thorac Surg 1985;40:494-497
© 1985 The Society of Thoracic Surgeons

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Articles

Fluorocarbons: A Potential Treatment of Cerebral Air Embolism in Open-Heart Surgery

From the Service de Chirurgie Cardio-Vasculaire, Hôpital Lariboisière, the Laboratoire de Physiologie et Physiopathologie Cérébro-Vasculaire (INSERM U-182, CNRS UA 641, UER Paris VII) and the Laboratoire de Neurophysiologie Ontogénétique, Paris, France, and the School of Public Health, Harvard University, Boston, MA.

^* Address reprint requests to Dr. Menasché, Service de Chirurgie Cardio-Vasculaire, Hôpital Lariboisière, 2, rue Ambroise Paré, 75010 Paris, France

This study was designed to assess whether an oxygenated fluorocarbon solution could reduce ischemic brain damage related to arterial air embolism. Air embolism was produced by injecting air bubbles into the carotid artery of barbiturate-anesthetized rats breathing 100% oxygen. Results were assessed on electrocorticogram. In an additional set of experiments, mass spectrometry was used to provide continuous monitoring of intracerebral tissue oxygen (PO ₂) and carbon dioxide (PCO ₂) tensions and intermittent measurement of cerebral blood flow (CBF). Fluorocarbon or saline solution (containing the emulsifying agent of fluorocarbons) was given intravenously after the initial air embolism (0.2 ml), and injections of air (0.1 ml) were repeated thereafter every five minutes.

The maximal amount of air required to achieve complete and irreversible flattening of the electrocorticogram was 1.60 ± 0.06 ml (mean ± standard error of the mean) in the saline-treated rats and 5.20 ± 0.44 ml in the fluorocarbon-treated group (p < 10^-7). In the second experiment, air embolism caused CBF to rise in both groups, the average percent of increase being higher in treated (41.6%) than in control animals (38.3%) (p < 0.02). However, in the control group, the increase in CBF did not prevent intracerebral tissue PO ₂ from decreasing by 7.4 ± 7.0% over the same period; conversely, in the fluorocarbon group, PO ₂ levels fell by only 2.5 ± 3.7% (p < 0.001 versus controls), but this time-averaged percentage was calculated over a longer period of cumulative ischemia because of the greater number of air emboli tolerated by treated animals.

We conclude that fluorocarbons seem to be effective in extending the tolerance of the brain to ischemic damage secondary to air embolism. Their protective mechanism most likely involves increased availability of oxygen for ischemic tissues and possibly indirect reduction of the size of air bubbles through enhanced denitrogenation of blood.

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