British journal of anaesthesia
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Low positive end-expiratory pressure (PEEP) can result in alveolar derecruitment, and high PEEP or high tidal volume (VT) in lung overdistension. We investigated cardiogenic oscillations (COS) in the airway pressure signal to investigate whether these oscillations can assess unfavourable intratidal events. COS induce short instantaneous compliance increases within the pressure-volume curve, and consequently in the compliance-volume curve. We hypothesised that increases in COS-induced compliance reflect non-linear intratidal respiratory system mechanics. ⋯ Heartbeat-induced oscillations within the course of the inspiratory pressure-volume curve reflect non-linear intratidal respiratory system mechanics. The analysis of these cardiogenic oscillations can be used to detect intratidal derecruitment and overdistension and, hence, to guide PEEP and VT settings that are optimal for respiratory system mechanics.
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Prothrombin complex concentrate (PCC) is increasingly used to correct acquired coagulopathy in trauma and surgery. Dosing of PCC is guided by the prothrombin time, which only reflects the onset of thrombin generation, but does not account for variations in intrinsic pathway coagulation factors, including factor IX (FIX). We hypothesised that FIX contained in PCC could strongly influence thrombin generation patterns. ⋯ FIX derived from PCC strongly enhances tissue factor-triggered thrombin generation in the presence of elevated FVIII activity. Haemodilution further enhances procoagulant effects of FIX and FVIII by slowing down inhibition of procoagulant enzymes. Dosing of PCC per prothrombin time may underestimate PCC's procoagulant potential because it does not account for intrinsic tenase or antithrombin activity.
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The metastatic potential of breast cancer cells has been strongly associated with overexpression of the chemokine CXCL12 and the activity of its receptor CXCR4. Lidocaine, a local anaesthetic that can be used during breast cancer excision, inhibits the growth, invasion, and migration of cancer cells. We therefore investigated, in a breast cancer cell line, whether lidocaine can modulate CXCL12-induced responses. ⋯ At clinical concentrations, lidocaine significantly inhibits CXCR4 signalling. The results presented shed new insights on the molecular mechanisms governing the inhibitory effect of lidocaine on cell migration.