P Pu ur rp po os se e: : The aim of this study was to evaluate the effectiveness of lidocaine, propofol and ephedrine in suppressing fentanyl-induced cough.M Me et th ho od ds s: : One hundred and eighteen patients were randomly assigned into four groups and the following medications were given intravenously: patients in Group I (n = 31) received normal saline 2 mL, Group II (n = 29) received lidocaine 2 mg·kg and Group IV (n = 28) received ephedrine 5 mg. At one minute after the study medication, fentanyl 2.5 µg·kg -1 was given intravenously within two seconds. The occurrence of cough and vital sign profiles were recorded within two minutes after fentanyl bolus by an anesthesiologist blinded to study design.R Re es su ul lt ts s: : Sixty-five percent of patients in the placebo group had cough, whereas the frequency was significantly decreased in Groups II (14%) and IV (21%). Although a numerically lower frequency of cough was noted in Group III (37%), it was not statistically different from that of the placebo group. SpO 2 decreased significantly in patients of Group III compared to placebo; one patient experienced hypoxemia necessitating mask ventilation. Patients in Group III showed a decrease in heart rate and systolic blood pressure (2 beats·min

The interaction between morphine and nalbuphine in PCA admixture on analgesia is additive. Combinations of morphine and nalbuphine in PCA can decrease the incidence of pruritus, and the antipruritus effect is ratio-dependent. This may provide a novel combination strategy of opioid agonist and agonist-antagonist for postoperative pain management after gynaecologic surgery.

Background Remote ischemic preconditioning (RIPC) initiates endogenous protective pathways in the brain from a distance and represents a new, promising paradigm in neuroprotection against cerebral ischemia-reperfusion (I/R) injury. However, the underlying mechanism of RIPC-mediated cerebral ischemia tolerance is complicated and not well understood. We reported previously that preactivation of Notch1 mediated the neuroprotective effects of cerebral ischemic preconditioning in rats subjected to cerebral I/R injury. The present study seeks to further explore the role of crosstalk between the Notch1 and NF-κB signaling pathways in the process of RIPC-induced neuroprotection. Methods Middle cerebral artery occlusion and reperfusion (MCAO/R) in adult male rats and oxygen-glucose deprivation and reoxygenation (OGD/R) in primary hippocampal neurons were used as models of I/R injury in vivo and in vitro, respectively. RIPC was induced by a 3-day procedure with 4 cycles of 5 min of left hind limb ischemia followed by 5 min of reperfusion each day before MCAO/R. Intracerebroventricular DAPT injection and sh-Notch1 lentivirus interference were used to inhibit the Notch1 signaling pathway in vivo and in vitro, respectively. After 24 h of reperfusion, neurological deficit scores, infarct volume, neuronal apoptosis, and cell viability were assessed. The protein expression levels of NICD, Hes1, Phospho-IKKα/β (p-IKK α/β), Phospho-NF-κB p65 (p-NF-κB p65), Bcl-2, and Bax were assessed by Western blotting. Results RIPC significantly improved neurological scores and reduced infarct volume and neuronal apoptosis in rats subjected to I/R injury. OGD preconditioning significantly reduced neuronal apoptosis and improved cell viability after I/R injury on days 3 and 7 after OGD/R. However, the neuroprotective effect was reversed by DAPT in vivo and attenuated by Notch1-RNAi in vitro. RIPC significantly upregulated the expression of proteins related to the Notch1 and NF-κB pathways. NF-κB signaling pathway activity was suppressed by a Notch1 signaling pathway inhibitor and Notch1-RNAi. Conclusions The neuroprotective effect of RIPC against cerebral I/R injury was associated with preactivation of the Notch1 and NF-κB pathways in neurons. The NF-κB pathway is a downstream target of the Notch1 pathway in RIPC and helps protect focal cerebral I/R injury.

Background: Peripheral intravenous catheters (PVCs) are widely used vascular access devices for infusion therapy; however, they are associated with relatively high failure rates. This study aimed to identify the incidence, risk factors and medical costs of PVC-induced complications in adult hospitalised adult patients in China. Methods: An observational, prospective study on 1069 patients lasting 5 months was conducted at a tertiary teaching hospital. Results: Infiltration ranked first among PVC complications with an incidence of 17.8%, followed by occlusion (10.8%) and phlebitis (10.5%). Most complications in phlebitis (88.4%) and infiltration (93.7%) were Grade 1. Catheters left in for over 96 h did not show a higher incidence of complications. Patients from the surgical department were more susceptible to infiltration, phlebitis and occlusion. The 26 gauge (Ga) catheters decreased the risk of phlebitis and occlusion, whereas 24Ga catheters increased infiltration rates. Infusing irritant drugs increased phlebitis and infiltration rates. The presence of comorbidities and non-use of needleless connectors were associated with occlusion. Compared with forearm insertion, the risk of occlusion nearly doubled with the dorsum of the hand insertion and the risk of infiltration tripled with antecubital fossa insertion. Medical treatment costs for PVC complications ranged from 0.3 to 140.0 CNY. Conclusions: Infiltration is the most common PVC-related adverse event. Clinically-indicated instead of routine replacement of catheters is safe. More efforts are warranted to improve nurses’ adherence to recent guidelines in terms of insertion site selection and needleless connector utilisation to reduce medical costs associated with catheter replacement.