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From the Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain.
Address correspondence to: Dr. Juan C. de la Pinta, Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Av Reyes Catolicos 2, Madrid 28040, Spain. Phone: 91 550 48 00; Fax: 91 549 47 64; E-mail: jcpinta{at}fjd.es
Purpose: There are several reports suggesting that volatile anesthetics alter vascular endothelial function. We analyzed the effect of sevoflurane, a fluorinated volatile anesthetic, on nitric oxide (NO)-dependent relaxation, evaluating the role of the endothelium-derived vasoconstrictor endothelin-1 (ET-1).
Methods: The experiments were performed in rat isolated aortic segments aerated in the absence and in the presence of sevoflurane (2%).
Results: Acetylcholine–induced relaxation was reduced in aortic segments aerated with sevoflurane. Sevoflurane failed to modify relaxatation in response to an exogenous NO donor, sodium nitroprusside. Superoxide dismutase, a scavenger of superoxide anion, partially restored the impaired vasorelaxation induced by sevoflurane, an effect that was associated with the release of superoxide anion. The presence of BQ-123, an antagonist of endothelin ETA-type receptors, normalized the vasorelaxing response to acetylcholine in the presence of sevoflurane. In addition, BQ-123 also reduced the ability of the sevoflurane-incubated vascular wall to release superoxide anion.
Conclusions: Our results suggest that sevoflurane impairs the endothelium-dependent vasorelaxation but that the endothelium-independent response remains intact. ET-1 and superoxide anion are involved in the endothelial dysfunction induced by sevoflurane. Further studies are needed to associate the endothelial dysfunction related to sevoflurane shown herein and its reported preconditioning properties on the myocardium.
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