A study of plasma atracurium and laudanosine concentrations was undertaken in 14 critically ill patients who received a bolus dose of atracurium 0.6 mg kg-1 followed by an infusion of 0.6 mg kg-1 h-1 for a period of 11-47 h. Seven of the patients had normal renal function and seven were in acute renal failure. In both groups plasma concentrations of atracurium reached a plateau of approximately 1300 ng ml-1 within 30 min of the bolus dose. The drug disappeared from the plasma within 120 min after discontinuation of the infusion. There was no difference between the two groups with respect to the pharmacokinetic parameters derived for atracurium. In the patients with normal renal function, plasma laudanosine concentration reached a plateau of approximately 1200 ng ml-1 within 10 h. In patients with renal failure there was a greater variation in the plasma laudanosine concentration: the highest value recorded was 4300 ng ml-1. Patients with renal failure had a significantly longer mean elimination half-life for laudanosine (1418 min v. 375 min; P less than 0.05) and Vd (4.52 litre kg-1 v. 2.40 litre kg-1; P less than 0.01) than the patients with normal renal function.

Neostigmine 1.25 mg or 0.625 mg was used to antagonize neuromuscular blockade produced by either atracurium 0.5 mg kg-1 or vecuronium 0.1 mg kg-1 in four groups of patients (n = 45) when the first EMG response of the train-of-four (A') had recovered to 10% of control (A). The time for A'/A and the train-of-four ratio (D'/A') to reach 70% was recorded. It was found that, after both atracurium and vecuronium, neostigmine 1.25 mg considerably accelerated recovery and, when compared with previous results, differed little from neostigmine 5.0 mg or 2.5 mg. Neostigmine 0.625 mg also significantly accelerated recovery after atracurium and was comparable to neostigmine 1.25 mg. However, with neostigmine 0.625 mg after vecuronium, recovery of D'/A' (but not A'/A) was little faster than spontaneous. Neostigmine 1.25 mg appears to be almost as effective as neostigmine 5.0 mg or 2.5 mg in antagonizing considerable block (90% depression of twitch height) produced by either atracurium or vecuronium, but neostigmine 0.625 mg is not sufficient, especially after vecuronium.

Propofol is the most commonly used compound for the intravenous induction and maintenance of anesthesia. Propofol addiction and abuse have become causes for concern in the healthcare community, especially among anesthesia and surgical professionals. The US Drug Enforcement Administration does not list propofol on any Schedules and most hospitals do not have inventory controls in place to prevent its misuse. Propofol is detectable in blood plasma as the parent compound for as much as 15 hours post-anesthesia. The metabolite propofol glucuronide (PPFG) has been detected in blood and urine as far out as 60 hours. Here we report the long-term renal excretion of PPFG in specimens from A) four participants following a 14-day course of orally ingested propofol dosing, and B) a female patient following anesthetic induction and 15 minutes' maintenance with propofol. Urinary PPFG was measurable well above limits of quantitation up to 6 days following oral ingestion and 28 days post-anesthesia. We also present a third set of data evaluating the likelihood of passive exposure to aerosolized propofol in the surgical environment by analyzing the levels of urinary PPFG of healthcare workers following operating room work shifts. The results presented here demonstrate that quantitation of PPFG in urinary samples is an efficient method of long-term screening for propofol misuse and abuse.

Recovery from neuromuscular block produced by vecuronium was studied in 50 patients using electromyography and the train-of-four technique. Twenty patients received neostigmine 2.5 mg, 10 when the initial response of the train-of-four was 50% of control and 10 when it was 10%. Neostigmine 5 mg was investigated in a similar manner and in 10 patients spontaneous recovery was studied. In all patients the time to 70% recovery of the initial response and of the train-of-four ratio was followed. Neostigmine significantly reduced the time to 70% recovery of both ratios with both degrees of block, but neostigmine 5.0 mg did not give a substantially more rapid recovery than 2.5 mg. No evidence of a neostigmine-induced block was encountered. neostigmine 2.5 mg was rapidly effective in antagonizing vecuronium-induced block, even when initial recovery was only slight: there was no advantage in using neostigmine 5.0 mg.