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.