British journal of anaesthesia
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It has repeatedly been shown that female patients wake up faster from propofol anaesthesia than male patients. The reason for this is not clear. It is possible that female patients have a more rapid decline in plasma propofol concentration after termination of an infusion, or there could be gender differences in the sensitivity to propofol, making women wake up at higher concentrations. We tested the hypothesis that women wake up faster because of a more rapid decline in plasma propofol. ⋯ The female patients had a more rapid decline in plasma propofol at the end of infusion. Gender differences in pharmacokinetics could explain the faster emergence for female patients after propofol anaesthesia, and gender differences in propofol sensitivity may also be present.
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Propofol is used during living-related donor liver transplantation because its metabolism is not greatly affected by liver failure. However, the pharmacokinetics of propofol during liver transplantation have not been fully defined. The purpose of this study was to evaluate the apparent systemic clearance of propofol during the dissection, anhepatic and reperfusion phases of living-related donor liver transplantation, and to estimate the role of the small intestine and lung as extrahepatic sites for propofol disposition. ⋯ Apparent systemic clearance was decreased by approximately 42 (10)% during the anhepatic phase compared with the dissection phase. After reperfusion, liver allografts rapidly began to metabolize propofol. The small intestine also participates in the metabolism of propofol.
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Case Reports
Treatment of cardiogenic shock with levosimendan in combination with beta-adrenergic antagonists.
Levosimendan, a calcium sensitizer, was used in combination with beta-adrenergic antagonists in a man aged 56 yr with cardiogenic shock, complicating acute myocardial infarction, who developed severe tachycardia after dobutamine administration. The patient's trachea was intubated, his lungs were ventilated, and he was started on dopamine 5 microg kg(-1) min(-1) and dobutamine 5 microg kg(-1) min(-1), titrated to a mean arterial pressure > or =65 mm Hg. He progressively became tachycardiac (>120 beats min(-1)) with a cardiac index (CI) of 1.4 litre min(-1) m(-2) despite adequate preload. ⋯ Subsequently, HR decreased over time and both catecholamines were discontinued 14 h after starting levosimendan infusion. The trachea was extubated within 20 h and the patient was discharged to the ward on day 4 after admission. In conclusion, levosimendan in combination with a beta-adrenergic antagonist may have beneficial effects in patients with cardiogenic shock who exhibit tachycardia in response to inotropic agents.
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This study determined the landmarks for caudal epidural block (CEB) after morphometric measurements of the sacral hiatus on dry sacral bones. Anatomical features of the sacral hiatus of clinical importance during CEB, along with distances and angles of use in detecting the apex, were measured. This provides detailed knowledge of the anatomy of the sacral hiatus and practical landmarks. ⋯ The triangle formed between the apex of the sacral hiatus and the superolateral sacral crests was found to have the features of an equilateral triangle. The sacrum and sacral hiatus are variable anatomical structures. However, the equilateral triangle located between the apex of the sacral hiatus and superolateral sacral crests will certainly be of use in determining the location of the sacral hiatus during CEB.
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We tested the hypothesis that isoflurane induces late preconditioning in cultured rat cortical neurones and preconditioning elicits changes in expression of Kir6.2 (the ion-conducting subunit of the metabolically responsive ATP-sensitive potassium (K(ATP)) channel) and EAAC1 (neuronal glutamate transporter). ⋯ Isoflurane induced late preconditioning in cultured rat cortical neurones. Ischaemic and pharmacological preconditioning with diazoxide and isoflurane induced ischaemic tolerance in the cultured neurones via mitoK(ATP) channels without an increase in Kir6.2 expression, and induced upregulation of EAAC1 expression.