Background and objective Polymorphonuclear leucocytes make a decisive contribution to defence against bacterial infections. In particular, the effects of anaesthetics on non-oxidative bactericidal mechanisms have previously only been superficially examined. Although the influence of anaesthetic agents on oxi-dative bactericidal activity has been thoroughly examined, our study concentrated on the effect on non-oxidative processes, which appears to have been a neglected field of research.

Methods The effects of methohexital, etomidate, ketamine, fentanyl and morphine on the activity of lysozyme and β-glucuronidase released from polymorphonuclear leucocytes have been studied in vitro. The activity of lysozyme was determined by recording the changes in the turbidity of a suspension of micro-coccus lysodeicticus caused by the enzymatic action of lysozyme. β-glucuronidase activity was photometrically measured by the enzymatic cleavage of phe-nolphthalein glucuronic acid.

Results High concentrations of methohexital inhibited lysozyme activity; however, etomidate and morphine caused an increase of β-glucuronidase activity in therapeutic plasma concentrations. While there was no effect of etomidate on lysozyme activity, all concentrations tested significantly stimulated β-glucuronidase activity. This result was unexpected because intravenous anaesthetics have previously shown a tendency to suppress polymorphonuclear leucocyte functions. Whereas the inhibition of lysozyme activity by the high concentration of methohexital was no surprise, the increase of β-glucuronidase activity caused by etomidate, ketamine, fentanyl and morphine was quite unexpected.

Conclusions At present, the underlying mechanism for the increase of β-glucuronidase activity caused by etomidate, ketamine, fentanyl and morphine is unknown. The fact that there was no influence of these agents on lysozyme activity possibly suggests that the anaesthetic agents have different effects on azurophilic and specific granules. Since in vitro investigations have their limitations, it is too early to draw practical consequences from our study. Moreover, at present it is unclear whether an increase of β-glucuronidase activity in vivo is an advantage or not. In any case, we think it advisable to perform further investigations on the influence of anaesthetic agents on oxygen-independent bactericidal mechanisms.

In order to compare the effect of atropine and sodium chloride on the dynamic compliance of the respiratory system after tracheal intubation, we studied 20 patients allocated randomly into two groups to receive either: atropine after 5 min of steady state and sodium chloride after 10 min (group A) or in reverse order (group B) intravenously. The study was conducted in a randomized double-blinded manner. The patients were anaesthetized with thiopental 5 mg kg−1 followed by thiopental 50 mg intravenously, as required. Intubation was facilitated by atracurium 0.5mg kg−1 intravenously and fentanyl 200 μg intravenously. During fixed volume ventilation (100 mL kg−1, f=10), compliance and end-tidal carbon dioxide were measured every 10 s by a Datex AS/3-respiratory module connected to a portable IBM-pc. Five minutes was allowed to establish a steady state then either atropine or sodium chloride was administered according to the protocol. Respiratory dynamic compliance increased significantly after intravenous administration of atropine (P < 0.05). We conclude that atropine 1.0 mg given intravenously provides protection against an intubation-induced decline in respiratory dynamic compliance.

Monocytes play a very important part in humoral as well as in cell-mediated immunity. At present, however, the knowledge of the influence of anaesthetic agents on the functions of monocytes is limited. In the present study, the effects of thiopentone, methohexitone, ketamine, midazolam, droperidol, propofol, etomidate, and fentanyl on monocyte chemotaxis were examined in vitro using a 48-well microchemotaxis chamber. Clinically relevant concentrations of ketamine, midazolam, and droperidol significantly (P≤0.05) inhibited chemotaxis. For that reason, it is possible that these anaesthetics impair the immunological system in vivo. This possibility should be further examined.

Gamma hydroxybutyric acid, a central inhibitory neurotransmitter and a cerebral metabolite of gamma-aminobutyric acid, is present in high concentrations in the mammalian hypothalamus and basal ganglia. Its sodium salt gamma hydroxybutyrate has been effectively used as an intravenous anaesthetic agent, and as an oral sedative, and in the management of the alcohol withdrawal syndrome. In an animal model, using 72 Wistar strain rats allocated to one of six groups of 12 animals each, with implanted lumbar intrathecal catheters, we examined whether gamma hydroxybutyrate, 20% 40 μL (32 mg kg−1) administered alone or combined with fentanyl, gamma hydroxybutyrate 20% 20 μL (16 mg kg−1), fentanyl 0.005% 20 μL (4 mg kg−1) as an intrathecal bolus, provides intra-operative anaesthesia, comparable with that produced by intrathecal lignocaine. We demonstrated that gamma hydroxybutyrate, given by an intrathecal bolus in the rat model, produced reversible segmental antinociception, together with muscular relaxation of the abdominal wall and rear limbs. This is accompanied by moderate sedation without haemodynamic or respiratory depression. This agent may thus be promising for use as a spinal anaesthetic drug.

One may have to use a monitor of cortical suppression to maintain the optimal level of sedation and hypnosis. The bispectral index (BIS), a processed EEG parameter, which incorporates coupling along with the frequency and amplitude of EEG waveforms, has been proposed as a measure of the pharmacodynamic anaesthetic effect on the central nervous system. The numerical value of BIS varies from 0 to 100 (no cerebral activity to fully awake patient). In order to achieve the desired level of propofol sedation or hypnosis, a target concentration of propofol at the effect site or in the blood must be delivered. Alternately, one may use BIS monitoring to monitor hypnosis or sedation levels or to reflect propofol concentrations in the blood. Significant correlations between plasma propofol concentrations and BIS values (r=0.68–0.78) have been reported by many investigators. During propofol-induced sedation, BIS values may be maintained above 75 to prevent airway obstruction and hypoxia. During propofol intravenous anaesthesia, BIS values from 40 to 60 have been proposed to maintain the desired level of hypnosis, with values below 50 associated with an insignificant probability of recall. However, the major limitation of the BIS monitor (monitor of hypnosis) relates to the fact that balanced anaesthesia comprises hypnosis, areflexia and analgesia and requires the administration of hypnotic agents, muscle relaxants and analgesics to achieve the desired clinical effects. Therefore, besides using the BIS value guidelines, one may also consider the haemodynamic, autonomic and somatic responses of the patient, the anaesthetic technique and the surgical interventions before deriving definite conclusions about the overall anaesthetic state of the patient.