This study was conducted to determine whether lignocaine or remifentanil effectively attenuate the response to endotracheal intubation during rapid sequence induction. Forty-eight patients were randomly divided into three groups: Group NS (n=16) received normal saline 0.1 ml/kg, Group L (n=16) received lignocaine 1.5 mg/kg, and Group R (n=16) received remifentanil 1 μg/kg. Anaesthesia was induced with propofol 2 mg/kg after glycopyrrolate 0.2 mg IV. Each study drug was given intravenously over 30 seconds after loss of consciousness. Cricoid pressure was applied until intubation. Succinylcholine 1.0 mg/kg was administered to facilitate tracheal intubation. After intubation, the patient's lungs were ventilated with sevoflurane 1% and nitrous oxide 50% in oxygen. Mean arterial pressure and heart rate were recorded before induction, at loss of consciousness, immediately before laryngoscopy and every minute after intubation for 10 minutes. Mean arterial pressure fell following propofol in all groups. The maximum increase in mean arterial pressure in Group NS and Group L were 46% and 38% respectively above the baseline value one minute after intubation, whereas the mean arterial pressure in Group R increased only back to the baseline value. Heart rate in Group NS and Group L were increased by 27% and 33% above baseline value respectively one minute after intubation, while that in Group R was increased only to the baseline value. The results indicate that remifentanil 1 μg/kg, but not lignocaine 1.5 mg/kg, effectively attenuates the haemodynamic response to endotracheal intubation during rapid sequence induction using propofol.
Despite aggressive clinical treatment, recurrence of glioblastoma multiforme (GBM) is unavoidable, and the clinical outcome is still poor. A convincing explanation is the phenotypic transition of GBM cells upon aggressive treatment such as radiotherapy. However, the microenvironmental factors contributing to GBM recurrence after treatment remain unexplored. Here, it is shown that radiation‐treated GBM cells produce soluble intercellular adhesion molecule‐1 (sICAM‐1) which stimulates the infiltration of macrophages, consequently enriching the tumor microenvironment with inflammatory macrophages. Acting as a paracrine factor, tumor‐derived sICAM‐1 induces macrophages to secrete wingless‐type MMTV integration site family, member 3A (WNT3A), which promotes a mesenchymal shift of GBM cells. In addition, blockade of either sICAM‐1 or WNT3A diminishes the harmful effect of radiation on tumor progression. Collectively, the findings indicate that cellular crosstalk between GBM and macrophage through sICAM‐1‐WNT3A oncogenic route is involved in the mesenchymal shift of GBM cells after radiation, and suggest that radiotherapy combined with sICAM‐1 targeted inhibition would improve the clinical outcome of GBM patients.
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