Maternal cardiovascular changes and neonatal acid-base status were assessed in 29 healthy women undergoing elective lower segment Caesarean section under spinal anaesthesia. The patients were allocated randomly to one of three groups to receive an i.v. infusion of one of the following: ephedrine 1 mg min-1 (group E1: n = 10), ephedrine 2 mg min-1 (group E2: n = 9), or phenylephrine 10 micrograms min-1 (group P: n = 10). Invasive arterial pressure was monitored continuously and if hypotension occurred (defined as a 20% decrease from baseline, taken after i.v. preload administration), bolus doses of either ephedrine (6 mg in groups E1 and E2) or phenylephrine (20 micrograms in group P) were given. Only four patients became hypotensive in group E2, compared with eight patients in group E1 and nine patients in group P. The total time that the patients remained hypotensive was greatest in group P (P < 0.005), less in group E1 and least in group E2. Neonatal Apgar scores and acid-base profiles were similar in all three groups. In this study, an infusion of phenylephrine 10 micrograms min-1 with bolus doses of 20 micrograms was shown to be significantly less effective in maintaining systolic arterial pressure within 20% limits of baseline compared with an infusion of ephedrine 1 or 2 mg min-1 with bolus doses of 6 mg.

We studied 160 ASA I-II patients, anaesthetized with propofol by infusion, using either a manually controlled or target-controlled infusion system. Patients were anaesthetized by eight consultant anaesthetists who had little or no previous experience of the use of propofol by infusion. In addition to propofol, patients received temazepam premedication, a single dose of fentanyl and 67% nitrous oxide in oxygen. Each consultant anaesthetized 10 patients in sequential fashion with each system. Use of the target-controlled infusion resulted in more rapid induction of anaesthesia and allowed earlier insertion of a laryngeal mask airway. There was a tendency towards less movement in response to the initial surgical stimulus and significantly less movement during the remainder of surgery. Significantly more propofol was administered during both induction and maintenance of anaesthesia with the target-controlled system. This was associated with significantly increased end-tidal carbon dioxide measurements during the middle period of maintenance only, but recovery from anaesthesia was not significantly prolonged in the target-controlled group. With the exception of a clinically insignificant difference in heart rate, haemodynamic variables were similar in the two groups. Six of the eight anaesthetists found the target-controlled system easier to use, and seven would use the target-controlled system in preference to a manually controlled infusion. Anaesthetists without prior experience of propofol infusion anaesthesia quickly became familiar with both manual and target-controlled techniques, and expressed a clear preference for the target-controlled system.

Retrograde cerebral perfusion did not influence immediate post-arrest nasopharyngeal temperature or cerebral metabolic recovery. The low jugular bulb Po(2) suggests equivalent ischemia. These findings cast doubt on the effectiveness of retrograde cerebral perfusion as a metabolic adjunct to hypothermic circulatory arrest.

These data suggest that human neutrophils produce NO in response to ANCA but in a NOS-independent way. NO can be generated from a nonenzymatic interaction between hydrogen peroxide and arginine. We postulate that this is the predominant pathway of NO synthesis in neutrophils, since ANCAs are capable of inducing reactive oxygen species production from neutrophils.