British journal of anaesthesia
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The i.v. anaesthetic propofol produces bronchodilatation. Airway relaxation involves reduced intracellular Ca(2+) ([Ca(2+)](i)) in airway smooth muscle (ASM) and lipid rafts (caveolae), and constitutional caveolin proteins regulate [Ca(2+)](i). We postulated that propofol-induced bronchodilatation involves caveolar disruption. ⋯ These novel data suggest a role for caveolae (specifically caveolin-1) in propofol-induced bronchodilatation. Due to its lipid nature, propofol may transiently disrupt caveolar regulation, thus altering ASM [Ca(2+)](i).
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Emergency laparotomy is a common intra-abdominal procedure. Outcomes are generally recognized to be poor, but there is a paucity of hard UK data, and reports have mainly been confined to single-centre studies. ⋯ This study confirms that emergency laparotomy in the UK carries a high mortality. The variation in clinical management and outcomes indicates the need for a national quality improvement programme.
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Supraglottic airway devices (SADs) play an increasing role in airway management in clinical anaesthesia and emergency medicine. Until now, no data exist concerning the extent of oesophageal insufflation when oropharyngeal leak pressures are exceeded. ⋯ The use of SADs with inspiratory pressures of 20 mbar appears to be safe regarding the risk of intragastric insufflation. Higher inspiratory pressures should be strictly avoided.
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We evaluated the ability of an infrared photoplethysmography arterial waveform (continuous non-invasive arterial pressure, CNAP) to estimate arterial pulse pressure variation (PPV). We compared the ability of non-invasive PPV to predict fluid responsiveness with invasive PPV, respiratory variation of pulse contour-derived stroke volume, and changes in cardiac index induced by passive leg raising (PLR) and end-expiratory occlusion (EEO) tests. ⋯ Non-invasive assessment of PPV seems valuable in predicting fluid responsiveness.
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Store-operated Ca(2+) entry (SOCE) has been implicated in various pathological conditions of the heart including ischaemia/reperfusion and ventricular hypertrophy. This study investigated the effects of sevoflurane on SOCE. ⋯ Sevoflurane at concentrations of ≥2% significantly inhibits the SOCE activity and prevents the resultant cellular Ca(2+) overload that leads to hypercontracture in ventricular myocytes. This inhibitory action may be involved in the cardioprotective effect of sevoflurane against Ca(2+) overload-mediated injury.