Double-blind comparison of sevofluran vs propofol and succinylcholine for tracheal intubation in children.
(73/1774)
We have studied intubating conditions in 64 healthy children, aged 3-10 yr, undergoing adenotonsillectomy, in a double-blind, randomized study. Intubation was performed 150 s after induction using either 8% sevoflurane in nitrous oxide and oxygen or propofol 3-4 mg kg-1 with succinylcholine 2 mg kg-1. An anaesthetist blinded to the technique performed intubation and scored intubating conditions using Krieg and Copenhagen Consensus Conference (CCC) scores. The trachea was intubated successfully at the first attempt in all patients under clinically acceptable conditions, although scores were significantly better with propofol and succinylcholine. The sevoflurane technique cost 3.62 +/- 0.55 Pounds to completion of tracheal intubation, significantly more (P < 0.001) than the cost of propofol-succinylcholine and isoflurane (2.04 +/- 0.54 Pounds) when based on actual amount of drug used. This cost increased to 4.38 +/- 0.05 Pounds when based on whole ampoules, which is significantly more than the cost of sevoflurane (P < 0.001). (+info)
Effects of propofol on extracellular acidification rates in primary cortical cell cultures: application of silicon microphysiometry to anaesthesia.
(74/1774)
Propofol depresses both cerebral oxygen consumption and glucose utilization. We tested the hypothesis that these well described effects on brain metabolism are manifest by a reduction in neuronal acid production in vitro. The rate of extracellular acidification in primary cell cultures of rat cortical neurones was measured using a novel instrument (silicon microphysiometer) after stimulation with propofol 0.3, 3 and 30 micrograms ml-1. Intralipid 10% served as a control. Propofol 3 micrograms ml-1 caused a mean decrease of 1.51 (SEM 0.71)% in baseline acidification rate, which was significantly greater than that produced by 0.3 microgram ml-1 or Intralipid alone (P < 0.05). The reduction after stimulation with propofol 30 micrograms ml-1 was 4.68 (0.35)% of baseline rates and this in turn was significantly greater than that elicited by propofol 3 or 0.3 microgram ml-1, or Intralipid (P < 0.001). We have confirmed the depressant effect of propofol on cerebral metabolism and established that propofol inhibits neuronal acid excretion in vitro. (+info)
Augmentation of vecuronium-induced neuromuscular block during sevoflurane anaesthesia: comparison with balanced anaesthesia using propofol or midazolam.
(75/1774)
We have quantified the potentiating effects of 1.7% sevoflurane (n = 12) on vecuronium-induced neuromuscular block and compared the results with those obtained during balanced anaesthesia with propofol (n = 12) or midazolam (n = 12) in 36 patients. Neuromuscular function was monitored using an accelerograph and the train-of-four responses of the adductor pollicis muscle to ulnar nerve stimulation. Vecuronium 0.1 mg kg-1 was administered as an intubating dose, and maintenance doses of 0.02 mg kg-1 were administered on three occasions when T1/T0 had recovered to 25%. Thereafter, spontaneous recovery was monitored until complete. Times to 25% recovery of T1/T0 (DUR25) after an intubating dose of vecuronium did not differ between groups (mean 44.2 (SD 18.7) min for sevoflurane, 38.3 (7.5) min for propofol and 35.5 (9.5) min for midazolam). DUR25 values after each maintenance dose were 29.8 (9.5) min, 30.3 (10.4) min and 31.6 (10.7) min during sevoflurane anaesthesia, and were significantly longer than values for propofol (21.7 (6.0) min, 21.5 (5.8) min and 21.9 (5.8) min) and midazolam (20.0 (5.9) min, 19.3 (7.7) min and 19.8 (8.0) min) (P < 0.05) in each case). Recovery index25-75% and interval from T1/T0 = 25% to T4/T1 = 0.7 after the final dose of vecuronium were significantly prolonged by sevoflurane (28.3 (13.2) min and 42.7 (16.4) min) compared with propofol (17.6 (6.1) min and 26.6 (9.8) min) or midazolam (16.3 (9.4) min and 26.0 (10.2) min) (P < 0.05 in each case). (+info)
A multicentre comparison of the costs of anaesthesia with sevoflurane or propofol.
(76/1774)
Day-case anaesthesia requires rapidly eliminated anaesthetics which are relatively expensive. This multinational, multicentre European study assessed the relative costs of propofol or sevoflurane anaesthesia in 211 patients. Anaesthesia was induced and maintained with propofol in group 1, with propofol and sevoflurane in group 2, and with sevoflurane in group 3. Drug and delivery costs were calculated in US$. Induction of anaesthesia was fastest in groups 1 and 2, although spontaneous ventilation resumed earliest in group 3. Emergence times and times at which patients were fit for discharge were similar in all groups. Group 2 had the lowest costs based on actual drug use (mean $14.2 (SEM 0.8) vs $18.7 (0.8) and $17.3 (0.8) in groups 1 and 3, respectively). Anaesthetic drug wastage and disposable costs were highest in group 1 and lowest in group 3. Consequently, total costs were highest in group 1 ($31.9 (0.9)) compared with groups 2 ($19.7 (0.9)) and 3 ($18.8 (0.9)). Although we observed increased nausea and vomiting in groups 2 and 3 and reduced patient satisfaction in group 3, these differences should be balanced against the greater cost of propofol anaesthesia. (+info)
Comparison of sevoflurane-nitrous oxide and propofol-alfentanil-nitrous oxide anaesthesia for minor gynaecological surgery.
(77/1774)
We studied 44 patients undergoing minor gynaecological surgery, anaesthetized in random order with sevoflurane-nitrous oxide or propofol-alfentanil-nitrous oxide. Operating conditions, recovery and postoperative nausea and vomiting (PONV) were assessed. For postoperative analgesia, all patients were given ketoprofen 100 mg rectally at the end of anaesthesia. Patients and gynaecologists were equally satisfied with both anaesthetic techniques. Patients given propofol woke up (3.5 vs 6.5 min), became orientated (5.0 vs 7.5 min) and were able to walk (57 vs 69 min) significantly (P < 0.05) earlier than those given sevoflurane, but there were no differences in times to achieve home readiness (166 vs 149 min) or in psychomotor recovery between the two groups. Intrauterine bleeding and PONV were more common with sevoflurane (incidence of PONV 64%) than with propofol anaesthesia (incidence of PONV 5%). We conclude that propofol-alfentanil is preferable to sevoflurane in ultra-short anaesthesia for minor gynaecological surgery. (+info)
Effects of propofol on vascular reactivity in isolated aortae from normotensive and spontaneously hypertensive rats.
(78/1774)
We have investigated the effects of propofol 50 mumol litre-1 on contractile and relaxant responses in experimental hypertension and assessed endothelial modulation of these responses. Propofol attenuated norepinephrine-induced contraction of endothelium-intact and endothelium-denuded rings from both Wistar Tokyo (WKY) and spontaneously hypertensive rats (SHR). The effect was significantly greater in endothelium-intact aortae from SHR than in those from WKY rats. Propofol markedly attenuated AVP-induced contraction in aortae from both WKY and SHR. Propofol attenuation of norepinephrine contraction was also observed in rings from both SHR and WKY rats incubated with L-NAME. Propofol attenuation of norepinephrine contraction was suppressed by indomethacin in aortae from SHR but not in those from WKY rats. These results suggest that: (1) propofol attenuated vascular contraction of isolated aortae from SHR in part by a mechanism dependent on events distal to the receptor site (norepinephrine, arginine vasopressin); (2) the effect of propofol on contraction in SHR, observed in the presence of nitric oxide synthase inhibitors but not cyclooxygenase inhibitors, was consistent with either propofol induction of vasodilating cyclooxygenase metabolites from the endothelium or propofol inhibition of vasoconstricting cyclooxygenase metabolites. (+info)
Propofol anaesthesia in mice is potentiated by muscimol and reversed by bicuculline.
(79/1774)
We have examined the role of gamma-aminobutyric acid (GABA) neurones in propofol anaesthesia in mice using the righting reflex. Propofol i.p. increased the percentage of loss of the righting reflex in a dose-dependent manner with an ED50 value of 140 (95% confidence limits 123-160) mg kg-1 (n = 40; eight animals per dose, five doses per dose-response curve). The ED50 for propofol decreased significantly to 66 (58-75) mg kg-1 in the presence of the GABAA receptor agonist muscimol 1 mg kg-1 i.p. (n = 40) (P < 0.05). In contrast, the ED50 increased significantly to 240 (211-274) mg kg-1 in the presence of the antagonist bicuculline 5 mg kg-1 i.p. (n = 40) (P < 0.05). Our results suggest that propofol anaesthesia may be mediated, at least in part by GABA neurons. (+info)
Sevoflurane anaesthesia causes a transient decrease in aquaporin-2 and impairment of urine concentration.
(80/1774)
Sevoflurane anaesthesia is occasionally associated with polyuria, but the exact mechanism of this phenomenon has not been clarified. Aquaporin-2 (AQP2) is an arginine vasopressin (AVP)-regulated water channel protein localized to the apical region of renal collecting duct cells and is involved in the regulation of water permeability. To elucidate the effect of sevoflurane anaesthesia on urine concentration and AQP2, we have compared serum and urinary concentrations of AVP, AQP2 and osmolar changes during sevoflurane and propofol anaesthesia. General anaesthesia was induced with sevoflurane or propofol in 30 patients for a variety of major surgical procedures. Blood and urine samples were obtained from patients at baseline, and 90 and 180 min after induction of anaesthesia. AVP and AQP2 concentrations were measured by radioimmunoassay. In both groups, plasma and urinary concentrations of AVP increased similarly during anaesthesia although plasma osmolality remained unchanged. Although urinary AQP2 excretion in the propofol group increased together with changes in plasma and urinary AVP, urinary AQP2 was significantly lower at 90 min in the sevoflurane group. Urine osmolality in the sevoflurane group also showed a transient but significant decrease in parallel with suppression of AQP2. Our data suggest that sevoflurane anaesthesia transiently produced an impaired AQP2 response to an increase in intrinsic AVP. (+info)