We have studied the analgesic, respiratory, cardiovascular and sedative effects of alfentanil 30 micrograms kg-1 i.m. in two experiments in six healthy volunteers. In the first experiment, recordings were made up to 120 min after injection. Thresholds (sensory and pain) and pain-related evoked potentials (amplitude and latency) to cutaneous argon laser stimulation were used for quantitative assessment of onset, efficacy and duration of analgesia. Pain was significantly reduced from 5 to 60 min after injection. The onset phase of analgesia was faster than the recovery phase. In the second experiment, the alfentanil-induced analgesia was antagonized by naloxone 0.4 mg i.v. The reaction time to pain was prolonged significantly 15 min after injection, whereas the latency of the pain-related potential remained constant. No clinically significant changes were observed in respiratory and cardiovascular measurements.

Bupivacaine (0.5%) 20 ml was administered extradurally to six healthy volunteers. It was found that simultaneous application of 10 needles to the skin could evoke pain when analgesia was obtained to one needle stimulation. In addition, a laser beam was used as a quantitative technique to activate simultaneously many cutaneous nociceptors. For 7 h, thresholds (sensory and pain) and pain-evoked brain potentials (amplitude and latency) to laser stimulation were monitored and used for quantitative assessment of onset, efficacy and duration of analgesia at various dermatomes (C7, T8, T10, T12, L1, L3, S1). The onset time of analgesia was shortest and conduction delay longest at the dermatome related to the site of injection (L3). Full analgesia was obtained at L1, L3 and S1, although the peak efficacy at S1 was delayed for 120-180 min after injection. A minor effect was found at dermatome C7 approximately 60 min after injection.

The efficacy, duration, and spread of epidural morphine hypoalgesia were assessed by an experimentally induced pricking pain evoked by laser stimulation. Four mg of plain morphine was injected epidurally in 7 volunteers at the L2-L3 interspace. Thresholds to warmth and pain perception, and pain-evoked potentials were measured. In the first experiment, hypoalgesia was monitored each hour for 7 h at various dermatomes. Hypoalgesia was detected at S1 dermatome after 2 h, but 3 h elapsed before hypoalgesia could be detected at the L1, T12, T10, T8, and T6 dermatomes. No effect was found at C7. No conduction delay was found along the pain pathway during hypoalgesia. Hypoalgesia lasted more than 7 h at S1, whereas hypoalgesia could not be detected after 5 h at other dermatomes. In the second experiment, naloxone (0.8 mg i.v.) was injected 230 min after injection of epidural morphine, and the subsequent recording 10 min later showed that hypoalgesia had been partly reversed. The onset and duration of hypoalgesia are different for experimentally induced pain and clinical pain. Experimentally laser-induced pain has the advantage of being quantitative, and is, as such, useful to assess hypoalgesia, and to test the potency of narcotics.

In 20 patients subjected to craniotomy for supratentorial cerebral tumours, the haemodynamic changes during halothane and neurolept anaesthesia were evaluated by measuring mean arterial blood pressure (MABP) and cerebral arterio-venous oxygen content differences (AVDO2) repeatedly during the operation. Ten patients were given 0.5% halothane anaesthesia and ten patients neurolept anaesthesia. MABP, AVDO2 and PaCO2 were measured after induction of anaesthesia, before and after incision, after opening and closure of the dura, at the time of extubation and 1 h later. Concerning MABP and PaCO2, no significant difference between the two groups was found. In both groups an increase in MABP was observed after incision (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group) and in the neurolept group after extubation (P less than 0.01). In both groups a decrease in AVDO2 was observed after incision (P less than 0.01) and after extubation (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group). During the operation AVDO2 values were significantly higher in the neurolept group (P less than 0.05). The results indicate that even a moderate increase in MABP after incision during neuroanaesthesia affects AVDO2 values, suggesting an increase in cerebral blood flow. The study suggests that autoregulation of cerebral blood flow might be better preserved during neurolept anaesthesia. A state of hyperperfusion of the brain after extubation was unveiled in both groups.

SummaryThe present study demonstrates a previously unnoticed source of bacterial contamination of locally manufactured compressed air for medical use. Air samples were drawn into a specially constructed device. and bacterial contents were identiJied from growth on agar plates. Various factors contributing to bacterial contamination of compressed air during production are mentioned and preventive measures are discussed.