Metabolism of sodium nitroprusside in dogs awake and anesthetized with halothane.

Sodium nitroprusside (SNP) is rapidly metabolized to cyanide (CN) and thiocyanate (SCN). The authors determined the rates of CN and SCN production during SNP infusion sufficient to maintain blood pressure at 80 per cent of baseline in the dog awake and during halothane anesthesia. Each dog served as its own control. The endogenous whole-blood CN concentration was significantly lower in anesthetized dogs (0.6 nmol/ml) than awake dogs (1.8 nmol/ml). CN concentration increased similarly during SNP infusion in awake (4.5 nmol/ml) and anesthetized dogs (2.3 nmol/ml). In another group of dogs, whole-blood CN concentration decreased significantly due to halothane anesthesia. The regression coefficient was -0.21 nmol CN/ml/hr. There was no significant difference in plasma SCN concentration following infusion of SNP in both awake (33 nmol/ml) and anesthetized dogs (26 nmol/ml). The cause of this decreased blood CN concentration with or without SNP infusion during halothane anesthesia is not known.

Rheumatoid arthritis of the cricoarytenoid joints: an airway hazard.

The anesthesiologist must maintain a high index of suspicion for the presence of cricoarytenoid arthritis and vocal-cord fixation in the rheumatoid arthritic. He must be prepared to intubate the trachea blindly, attempting to minimize trauma by using a smaller endotracheal tube. Indirect laryngoscopy, or direct laryngoscopy using a fiberoptic laryngoscope, may be indicated as part of the preanesthetic evaluation. In some instances, preanesthetic tracheostomy or an alternative regional anesthetic technic may be appropriate. Unusually close vigilance in the postoperative period may be required to detect signs of postextubation airway obstruction.

Pharmacological activity, metabolism, and pharmacokinetics of glycinexylidide.

Glycinexylidide (GX) is a metabolite of lidocaine that is frequently present in mug/ml concentrations in the plasma of patients treated with lidocaine infusions for 24 hr or more. Plasma levels of GX have 26% the antiarrhythmic activity of lidocaine in an animal model, and GX adversely affects the mental performance of normal subjects at plasma concentrations comparable to those found in patients. The total volume of GX distribution in man is similar to that of lidocaine but the plasma clearance is less, so that the 10-hr elimination phase half-life of GX is much longer than the 1 1/2 hr half-life reported in normal subjects for lidocaine. About half of an administered dose of GX is excreted unchanged in urine, roughly 15% appears in urine as conjugates of xylidine and p-OH xylidine, and the fate of the rest is unknown.