ABSTRACT

Until the early 1960s, it was thought that the volatile anesthetic agents were not me­ tabolized to a significant degree by humans. The recognition that some patients who re­ ceived methoxyflurane as an anesthetic agent developed postoperative renal dys­ function and that the renal dysfunction might be related to a metabolite of me­ thoxyflurane was a major stimulus to an intensive study of the metabolism of me­ thoxyflurane. This culminated in the rec­ ognition that the etiology of the methoxyflurane-induced renal dysfunction was due to metabolism of methoxyflurane and the release of inorganic fluoride (F _), a known nephrotoxin. Recognition of the impor­ tance of metabolism to anesthesia-induced toxicity was the stimulus to a major and continuing research effort into the metabo­ lism and toxicity of all the volatile anes­ thetic agents.