European journal of anaesthesiology
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We do not know how general anaesthetics cause their desired effects. Contrary to what has been thought until relatively recently, the clinical state of anaesthesia consists of multiple components that are mediated via interaction of the anaesthetic drugs with different targets on the molecular, the cellular, the network and the structural-anatomical levels. The mechanisms by which some of these drugs induce the different components of "anaesthesia" may be rather specific: discrete mutations of single amino acids in specific proteins profoundly affect the ability of certain anaesthetics to achieve specific endpoints. ⋯ This article will focus on evidence for anaesthetic toxicity in the central nervous system, which appears to be susceptible to anaesthetic neurotoxicity primarily at the extremes of ages but via different pathways: in the neonate, during the period of most intense synaptogenesis, anaesthetics can induce excessive apoptosis; in the aging brain subtle cognitive dysfunction can persist long after clearance of the drug and processes resembling neurodegenerative disorders may be accelerated. At all ages, anaesthetics affect gene expression regulating protein synthesis in poorly understood ways. While it seems reasonable to assume that the vast majority of our patients completely restore homeostasis after general anaesthesia, exposure to these drugs probably has more profound and longer-lasting effects on the brain than heretofore imagined.
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It is widely accepted that sevoflurane affects cerebral circulation, but there are uncertainities regarding the magnitude of its effect. The aim of the present work was to assess the effect of sevoflurane on the cerebral circulation at surgical levels of anaesthesia. ⋯ Our data indicate a vasodilatory effect of sevoflurane at surgical level of anaesthesia on large cerebral vessels or a vasoconstriction of the resistance arterioles likely caused by decreased brain metabolism.
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Randomized Controlled Trial Comparative Study
Parecoxib vs. lornoxicam in the treatment of postoperative pain after laparoscopic cholecystectomy: a prospective randomized placebo-controlled trial.
Non-steroidal anti-inflammatory drugs are considered as an effective treatment of postoperative pain after laparoscopic cholecystectomy. COX-2 inhibitors are newer drugs having less adverse effects. Data supporting their efficacy postoperatively in comparison to older non-steroidal anti-inflammatory drugs are scarce. Our study is a prospective, randomized, double-blinded, placebo-controlled trial comparing the efficacy of lornoxicam vs. parecoxib for the management of pain after laparoscopic cholecystectomy. ⋯ Parecoxib 40 mg i.v. and lornoxicam 8 mg i.v. were equianalgesic and both were more efficacious than placebo for the management of pain after laparoscopic cholecystectomy.
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Randomized Controlled Trial
Positive end-expiratory pressure does not affect indocyanine green plasma disappearance rate or gastric mucosal perfusion after cardiac surgery.
Positive end-expiratory pressure (PEEP) may affect hepato-splanchnic blood flow. We studied whether a PEEP of 10 mbar may negatively influence flow-dependent liver function (indocyanine green plasma disappearance rate, ICG-PDR) and splanchnic microcirculation as estimated by gastric mucosal PCO2 (PRCO2). ⋯ A PEEP of 10 mbar for 2 h does not compromise liver function and gastric mucosal perfusion in patients after cardiac surgery with maintained cardiac output.