Background and objective: Thiopental prolongs the QT interval more than propofol, and the two induction agents were compared in patients with subarachnoid haemorrhage predisposed to electrocardiographic abnormalities and cardiac dysrhythmias.

Methods: Twenty-nine patients were studied randomly. Anaesthesia was induced with either thiopental or propofol and fentanyl; vecuronium was used as a neuromuscular blocking agent. The electrocardiogram and arterial blood pressure were monitored from before the induction of anaesthesia to 2 min after endotracheal intubation.

Results: The median QT interval was at baseline 423 ms in the thiopental group and at 432 ms in the propofol group, and it increased in the thiopental group to 446 ms and decreased in the propofol group to 425 ms (P < 0.01 between groups). After induction and endotracheal intubation, the number of patients with increased QT dispersion was greater in the propofol group (P < 0.05). The incidence of cardiac dysrhythmias was similar in the study groups.

Conclusions: Thiopental and propofol are equally suitable for the induction of anaesthesia in patients with subarachnoid haemorrhage.

Background and objective: Thiopental in clinically relevant concentrations inhibits the oxidative function of neutrophils, whereas only very high, non-therapeutic concentrations of methohexital induce a similar effect. The study characterized the molecular basis of this differential action of oxy- and thiobarbiturates on neutrophils.

Methods: Neutrophils were incubated in vitro with thiopental or methohexital using concentrations within the therapeutic range. Neutrophil responses were induced using different stimuli: N-formyl-L-methionyl-Lleucyl-L-phenylalanine (FMLP), C5a and 1,2-dioctanoyl-sn-glycerol (DiC8-DAG). FMLP and C5a bind to specific G-protein-coupled receptors that share the same second messenger cascade. In contrast, DiC8-DAG, an activator of protein kinase C, bypasses the signal transduction pathway downstream of the receptors. Hydrogen peroxide production by neutrophils was assessed using flow cytometry. To characterize the localization of the interaction site, FMLP receptor expression and cytosolic-free calcium were further analysed.

Results: FMLP and C5a-induced hydrogen peroxide production were both significantly impaired by thiopental, but not by methohexital. When postreceptor signalling was bypassed, by stimulation with DiC8-DAG, neither thiopental nor methohexital affected hydrogen peroxide production. Additionally, neither of the barbiturates impaired the cytosolic Ca2+ response.

Conclusions: We conclude that neither protein kinase C nor the hydrogen peroxide-generating enzymes are affected by thiopental or methohexital. The unimpaired Ca2+ response suggests that the function of the receptors and G-proteins were also unimpaired. Taken together, this indicates that the site of action of thiopental is in the cellular signalling upstream of protein kinase C.

Background and objective: This prospective, randomized, double-blinded study was designed to compare the effects of remifentanil or fentanyl on anaesthetic induction characteristics of propofol, thiopental or etomidate.

Methods: Seventy-two patients were enrolled in six groups of 12 individuals each. In three groups, fentanyl was given as a bolus dose of 1.5 μg kg−1, whereas the others received a remifentanil infusion at 0.5 μg kg−1 min−1. Five minutes later, propofol, thiopental or etomidate were titrated to a state of unresponsiveness. Assessment included the amounts of drug necessary for induction, haemodynamics and the times to apnoea, loss of eyelash reflex, and the release of a water-filled syringe held in the patient's hand.

Results: Induction times to loss of the eyelash reflex were significantly shorter in the remifentanil than in the fentanyl groups: with propofol 50.7 ± 13.6 s (mean ± SD) versus 74.9 ± 27.0 s (P < 0.01), with thiopental 42.9 ± 16.8 s versus 77.2 ± 27.8 s (P < 0.01) and with etomidate 54.7 ± 17.6 s versus 72.3 ± 24.0 s (P < 0.05). The times to respiratory arrest or for the syringe to fall were significantly shorter with remifentanil than with fentanyl for propofol and for thiopental, but not for etomidate. In terms of dosages per kg body weight necessary to achieve unresponsiveness, less propofol (−29%, P < 0.05), thiopental (−25%, P < 0.05) or etomidate (−32%, P < 0.01) was necessary with remifentanil than with fentanyl. Haemodynamic responses to tracheal intubation were controlled more effectively with remifentanil. However, within the remifentanil groups, mean arterial pressure significantly decreased during induction: −26% with propofol,−18% with thiopental and −14% with etomidate (all P < 0.01).

Conclusions: During anaesthetic induction, a remifentanil infusion of 0.5 μg kg−1 min−1 over 5 min is a suitable alternative to a 1.5 μg kg−1 bolus dose of fentanyl: induction times are shorter with reduced amounts of propofol, thiopental or etomidate.

The choice of hypnotics and opioids for rapid-sequence induction, and the use of premedication, is influenced by the choice of the muscle relaxant. Anaesthetic agents have a major influence on the quality of intubation when rapid-sequence induction is achieved without a muscle relaxant. Premedication is important, along with a high dose of propofol (2.5 mg kg−1 or more) and a short-acting opioid such as alfentanil (30–40 μg kg−1) or remifentanil (up to 4 μg kg−1). It has also been demonstrated that i.v. lidocaine can improve intubating conditions. When a muscle relaxant is used, the choice of the anaesthetic agents depends on the onset of action of the relaxant. With a rapid-acting compound such as rocuronium at a dose of 0.6 mg kg−1, the hypnotic agents need to be supplemented with only a small dose of opioids, e.g. alfentanil 10–20 μg kg−1. When succinylcholine, rocuronium 1.0 mg kg−1 or rapacuronium 1.5 mg kg−1 are used, excellent intubating conditions may be obtained by relatively smaller doses of hypnotic agents even without opioids; however, haemodynamic and intraocular pressure changes are better controlled when small doses of opioids are administered.

Background and objective Respiratory burst is an essential component of the neutrophil's biocidal function. In vitro, sodium thiopental, isoflurane and lidocaine each inhibit neutrophil respiratory burst. The objectives of this study were (a) to determine the effect of a standard clinical induction/tracheal intubation sequence on neutrophil respiratory burst and (b) to determine the effect of intravenous lidocaine administration during induction of anaesthesia on neutrophil respiratory burst.

Methods Twenty ASA I and II patients, aged 18–60 years, undergoing elective surgery were studied. After induction of anaesthesia [fentanyl (2 μg kg−1), thiopental (4–6 mg kg−1), isoflurane (end-tidal concentration 0.5–1.5%) in nitrous oxide (66%) and oxygen], patients randomly received either lidocaine 1.5 mg kg−1 (group L) or 0.9% saline (group S) prior to tracheal intubation. Neutrophil respiratory burst was measured immediately prior to induction of anaesthesia, immediately before and 1 and 5 min after lidocaine/saline.

Results Neutrophil respiratory burst decreased significantly after induction of anaesthesia in both groups [87.4 ± 8.2% (group L) and 88.5 ± 13.4% (group S) of preinduction level (P < 0.01 both groups)]. After intravenous lidocaine (but not saline) administration, neutrophil respiratory burst returned towards preinduction levels, both before (97.1 ± 23.6%) and after (94.4 ± 16.6%) tracheal intubation.

Conclusion Induction of anaesthesia and tracheal intubation using thiopentone and isoflurane, inhibit neutrophil respiratory burst. This effect may be diminished by the administration of lidocaine.

The effects of propofol and thiopental on three vasoconstrictors, acetylcholine, histamine, and serotonin were studied in isolated porcine and human coronary artery rings. Propofol and thiopental attenuated the contractile response to all mediators in a dose-dependent manner. This dilating effect was fairly weak using low concentrations (propofol 1 μg mL−1 and 10 μg mL−1, thiopental 5 μg mL−1 and 10 μg mL−1). In the presence of high concentrations (propofol 100 μg mL−1, thiopental 50 μg mL−1) marked relaxation was observed (propofol −32% up to −49%, P < 0,05; thiopental −23% up to −67%, P < 0.05). These dilating effects were seen both in intact and denuded rings, the differences were not significant. Human coronary artery segments were relaxed by thiopental (−22% to −76%) and propofol (−11% to −67%) to a similar extent. Our data indicate that propofol and thiopental relax isolated coronary segments in a dose-dependent manner, and that there is no evidence that these effects are dependent of endothelial factors.

We studied the direct effect of intravenous anaesthetics, local anaesthetics and premedication drugs in common use for major surgery, on the spontaneous versus lectin induced proliferation of cultured normal rat peripheral blood mononuclear cells, not exposed to surgical or any other trauma prior to culture. Peripheral blood mononuclear cells were incubated in cell-culture medium in the presence or in the absence of propofol, ketamine, fentanyl, midazolam, thiopental sodium, lidocaine or etomidate. The cells proliferated either spontaneously or under stimulation with a lectin phytohaemagglutinine P for 72 h. The proliferation rate was evaluated by 2H-Thymidine incorporation. Fentanyl, thiopental sodium, lidocaine and etomidate significantly inhibited phytohaemagglutinine P induced 3H-Thymidine incorporation in cultured rat peripheral blood mononuclear cells. Counts per minute of the cultures treated with these drugs were 1667.80±745.72, 1614.1±615.00, 1688.0±615.0 and 1549±560.41, respectively, compared with the phytohaemagglutinine P stimulated positive control counts per minute, 13488±4305.6 (P<0.001 in each comparison). Propofol, ketamine and midazolam inhibited the lectin-induced cell proliferation to levels not statistically different from the baseline. Counts per minute of these cultures were 1361.90±745.73; 1108.90±751.33 and 1518.10±848.88, respectively. Compared either with the baseline 972.57±356.73 counts per minute or to the positive control culture counts per minute, 13488±4305.6 the difference was statistically significant (P<0.001) in each comparison. All the substances tested in this study proved capable of exerting direct inhibitory effect on circulating immunocompetent cells, because the latter were not subjected to any other immunosuppressive factor, be it operative trauma, blood transfusion, malnutrition, drug abuse, prior to culture. The possible theoretical and practical implications are discussed in this study.