Abstract
Purpose
Degradation of sevoflurane by carbon dioxide absorbents produces compound A, a vinyl ether. In rats, compound A can produce renal corticomedullary necrosis. We tested whether other compounds produced by sevoflurane degradation also could produce corticomedullary necrosis.
Methods
Two groups of rats were exposed for four hours to sevoflurane 2.5% delivered through a container filled with fresh Sodasorb® and heated to 30∘C or to 50∘C, respectively. Compound A was added to produce an average concentration of 120 ppm in both groups. A third (control) group received 2.5% sevoflurane that did not pass through absorbent, and no compound A was added.
Results
As determined by gas chromatography, the higher temperature produced more volatile breakdown products, including compound A. Median necrosis of the corticomedullary junction in the 50∘C group [10% (quartiles 1.096-7.8%); n = 20] exceeded that in the 30∘C group [5% (6.5%-15%); n = 18;P < 0.02], and both exceeded the median necrosis in the control group [0% (0.096-0.2%);n = 10;P < 0.02], The respective mean ± SD values for these three studies were: 12.8 ± 16.7%, 5.3 ± 4.4%, and 0.3 ± 0.5%.
Conclusion
Degradation products of sevoflurane other than compound A can cause or augment the renal injury in rats produced by compound A.
Résumé
Objectif
La dégradation du sévoflurane par les absorbants de gaz carbonique produit un éther vinylique, le composé A. Chez les rats, ce composé provoque une nécrose corticomédullaire rénale. Nous avons vérifié si d’autres composés issus de la dégradation du sévoflurane peuvent aussi provoquer cette nécrose.
Méthode
Deux groupes de rats ont été exposés pendant quatre heures à du sévoflurane à 2,5 % administré après avoir traversé un récipient rempli de Sodasorb® frais et chauffé respectivement à 30° C ou à 50°C. Du composé A a été ajouté pour produire une concentration moyenne de 120 ppm dans les deux groupes. Un troisième groupe (témoin) a reçu du sévoflurane à 2,5 %, qui ne traversait pas l’absorbant, et sans ajout de composé A.
Résultats
Les résultats de la Chromatographie en phase gazeuse ont montré que sous la température la plus élevée, il y a eu plus de produits de dégradation volatils, y compris le composé A. Dans le groupe 50°C, la nécrose moyenne de la jonction corticomédullaire dépassait [10 % (quartiles 1,0 %-7,8 %); n = 20] celle du groupe 30°C [5 %(6,5%- 15%);n = 18; P < 0,02] et les deux étaient plus élevée que celle du groupe témoin [0 % (0,0%-0,2 %); n = 10; P < 0,02]. Les valeurs respectives de la moyenne ± l’écart type ont été de 12,8 ± 16,7%, 5,3 ± 4,4 % et de 0,3 ± 0,5 %.
Conclusion
Les produits de dégradation du sévoflurane, autres que le composé A, peuvent causer ou augmenter la lésion rénale produite par le composé A chez les rats.
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Dr. Eger is a paid consultant to Baxter Healthcare Corporation. This study was not funded by Baxter Healthcare Corporation (nor by any other external source), who did, however, supply compound A for these studies.
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Stabernack, C.R., Eger, E.I., Warnken, U.H. et al. Sevoflurane degradation by carbon dioxide absorbents may produce more than one nephrotoxic compound in rats. Can J Anaesth 50, 249–252 (2003). https://doi.org/10.1007/BF03017793
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DOI: https://doi.org/10.1007/BF03017793