At clinically relevant concentrations, volatile anaesthetic agents influence neutrophil function. Our hypothesis was that sevoflurane would inhibit neutrophil apoptosis and consequently influence the postoperative pro-inflammatory state. In order to identify selectively the effect of the anaesthetic agent sevoflurane, we studied patients undergoing minimally stimulating (cataract) surgery randomly allocated to receive either sevoflurane (n=11) or local anaesthesia (n=12). Venous blood samples were taken immediately prior to anaesthesia and at 1, 8 and 24 h thereafter. The rate of neutrophil apoptosis, plasma concentration of cytokines and differential white cell count were measured. The rates of neutrophil apoptosis and plasma concentrations of IL-1β, TNF-α and IL-8 at each time point were similar in the two groups. IL-6 concentrations increased significantly and to a similar extent compared to preanaesthetic levels at 8 and 24 h. This study demonstrates that sevoflurane does not influence the rate of neutrophil apoptosis, cytokine concentrations and neutrophil count following cataract surgery.

The aim of this study was to elucidate the influence of four neuromuscular blocking substances on coronary vascular tone using the model of isolated porcine coronary artery segments. We studied the effects of four muscle relaxants, atracurium, pancuronium, rocuronium, and vecuronium (0.1, 1, and 10 μg mL−1 each), on the contractile response to three vasoconstrictors: acetylcholine, histamine, and serotonin. None of the neuromuscular blocking agents under investigation exerted a significant influence on the vasoconstricting effects of these mediators except for pancuronium, which dose-dependently attenuated acetylcholine-mediated contractions (−10.8% attenuation for 10 μg mL−1 pancuronium, P < 0.05). There was no difference between vessels with intact endothelium and denuded preparations. It is concluded that high-dose pancuronium exerts an antimuscarinic effect in vascular smooth muscle. The other neuromuscular agents studied do not alter vascular reactivity of isolated porcine coronary arteries.

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.

Postoperative renal impairment is a recognized complication of infrarenal aortic cross-clamping. Fenoldopam, a selective dopamine agonist, may increase renal blood flow and decrease tubular oxygen consumption. The objective of this study was to quantify the effects of fenoldopam (0.1 μg kg−1 min−1) on renal blood flow and renal tubular function in anaesthetized dogs that have undergone aortic cross clamping. Eight labrador dogs were selected to receive either saline or fenoldopam (0.1 μg kg−1 min−1) intravenously. Arterial pressure, heart rate, renal blood flow, urinary output, fractional excretion of sodium, creatinine clearance and lithium clearance were measured (a) prior to infusions of saline or fenoldopam (b) 1 h after commencing the infusion (c) during a 90 min period of infrarenal aortic cross-clamping with concurrent infusion of fenoldopam or saline and (d) for 1 h after simultaneous aortic declamping and discontinuation of the infusions. There was no haemodynamic instability upon commencing the infusion of fenoldopam (0.1 μg kg−1 min−1). Creatinine clearance (2.03±0.5–2.45±0.3 mL min−1 kg−1 (mean±SD)), urine output (0.23±0.16–0.35±0.23 mL min−1 (mean±SD)), and fractional excretion of sodium (0.7±0.52–1.3±0.73% (mean±SD)) increased (P < 0.05), following commencement of the fenoldopam infusion. Fractional excretion of sodium (1.2±0.7% (mean±SD)) and urine output (0.36±0.21 mL min−1 (mean±SD)) were maintained during the aortic cross-clamp period (P < 0.05). Renal blood flow increased when the fenoldopam infusion was commenced (145±43.3–161±39.2 mL min−1 (mean±SD)) and remained greater than baseline during the aortic cross-clamping period (152±44 mL min−1 (mean±SD)), although these increases did not reach statistical significance. The most striking abnormalities observed by electron microscopy were marked disruption of the microvillus brush border in proximal tubules, vacuolation and separation of epithelial cells on basolateral infolds. The changes were similar in the two groups. In conclusion fenoldopam (0.1 μg kg−1 min−1) may have renoprotective effects which persist during infrarenal aortic cross clamping.

This study investigated the changes in the hypnotic component of anaesthesia, estimated by the bispectral index of the electroencephalogram, during normothermic cardiopulmonary bypass. Twenty-six patients (20 men, 6 women), aged 61±11 years (Mean±SD) scheduled for cardiac surgery were premedicated with hydroxyzine and meperidine. Anaesthesia was induced and maintained with a computer-controlled continuous infusion (not adjusted for haemodilution) of sufentanil (effect site concentration 0.4–0.6 ng mL−1) and a manually adjusted continuous infusion of propofol (4.4±1.8 mg kg−1 h−1). Cardiopulmonary bypass was normothermic with moderate haemodilution. Bispectral index was measured with a referential montage before, 30 s, 1, and 3 min after cardiopulmonary bypass onset, before and after aortic cross-clamping, 30 min after cardiopulmonary bypass onset, before and after aorta cross-clamp release and before and after weaning from cardiopulmonary bypass. Bispectral index values were 48±8 before cardiopulmonary bypass onset, 50±10 before, and 48±8 after end of cardiopulmonary bypass (P=NS). No patient had increases in bispectral index values during cardiopulmonary bypass consistent with awakening. We conclude that with the anaesthetic regimen presented in this study bispectral index values do not change during normothermic cardiopulmonary bypass.

Clevidipine is a new lipophilic, ultra-short acting 1,4-dihydropyridine calcium channel antagonist for intraoperative use. Because sarcolemnal calcium currents are involved in the mechanism of action of anaesthetics we questioned whether clevidipine alters the potency of volatile anaesthetics. We studied the effects of clevidipine on minimal alveolar concentration and the time to awaken from isoflurane anaesthesia. Sprague-Dawley rats were anaesthetized with isoflurane, and were allocated to one of four treatments prior to minimal alveolar concentration determination: (a) saline control; (b) clevidipine 20 nmol kg−1 min−1; (c) clevidipine 40 nmol kg−1 min−1; (d) clonidine 1 μg kg−1 – positive control. Ten mongrel dogs were anaesthetized with isoflurane and received a continuous infusion of clevidipine 6 nmol kg−1 min−1 or the solvent (Intralipid 20% – control). After 2 h of steady-state anaesthesia, minimal alveolar concentration awake and the time to awakening were recorded. Clevidipine reduced minimal alveolar concentration to a small but statistically significant extent (from 1.40±0.16 control to 1.23±0.13 vol% with 20 nmol kg−1 min−1 and to 1.27±0.12 vol% with 40 nmol kg−1 min−1; mean±SD; P < 0.05) in rats. Clonidine reduced minimal alveolar concentration to 0.90±0.17 vol% (mean± SD; P < 0.05). Minimal alveolar concentration awake and the duration of sleep were not affected by clevidipine in dogs. Clevidipine mildly reduces miinimal alveolar concentration of isoflurane but does not prolong the duration of sleep and does not affect minimal alveolar concentration awake after a 2-h steady-state isoflurane anaesthesia.

The failure of anaesthetic equipment as a result of maintenance is extremely rare. The ingress of water into the flowmeters of an anaesthetic machine from the piped medical air supply is reported and is possibly unique. The piped medical air supply was open to the atmosphere during maintenance. Water condensed in the gas pipeline and this was not noticed during subsequent testing. Water was seen leaking from the orthopaedic air tools used for surgery but was assumed to be from the autoclaving process. Later the same day, when medical air from the piped source was used as part of the gas mixture for a general anaesthetic, water was seen filling the barrel of the flowmeter air control valve. This could have had far-reaching and dangerous consequences for the patient, which were fortunately averted.