Emergence agitation is common after nasal surgery. We investigated the effects of intraoperative dexmedetomidine infusion on emergence agitation and quality of recovery after nasal surgery in adult patients. One hundred patients undergoing nasal surgery were randomized into two groups. The dexmedetomidine group (Group D, n=50) received dexmedetomidine infusion at a rate of 0.4 μg kg(-1) h(-1) from induction of anaesthesia until extubation, while the control group (Group C, n=50) received volume-matched normal saline infusion as placebo. Propofol (1.5-2 mg kg(-1)) and fentanyl (1 μg kg(-1)) were used for induction of anaesthesia, and desflurane was used for maintenance of anaesthesia. The incidence of agitation, haemodynamic parameters, and recovery characteristics were evaluated during emergence. A 40-item quality-of-recovery questionnaire (QoR-40) was provided to patients 24 h after surgery. The incidence of agitation was lower in Group D than Group C (28 vs 52%, P=0.014). Mean arterial pressure and heart rate were more stable in Group D than in Group C during emergence (P<0.05). Time to extubation, bispectral index, and respiratory rate at extubation were similar between the groups. Global QoR-40 score at 24 h after surgery was higher in Group D (median [range], 183 [146 -198]) compared with Group C (178 [133-196]) (P=0.041). Intraoperative infusion of dexmedetomidine provided smooth and haemodynamically stable emergence. It also improved quality of recovery after nasal surgery.

Introduction: Perioperative anesthesia and analgesia exacerbate immunosuppression in immunocompromised cancer patients. The natural killer (NK) cell is a critical part of anti-tumor immunity. We compared the effects of two different anesthesia and analgesia methods on the NK cell cytotoxicity (NKCC) in patients undergoing breast cancer surgery.

Pericytes are believed to originate from either mesenchymal or neural crest cells. It has recently been reported that pericytes play important roles in the central nervous system (CNS) by regulating blood-brain barrier homeostasis and blood flow at the capillary level. However, the origin of CNS microvascular pericytes and the mechanism of their recruitment remain unknown. Here, we show a new source of cerebrovascular pericytes during neurogenesis. In the CNS of embryonic day 10.5 mouse embryos, CD31⁺F4/80⁺hematopoietic lineage cells were observed in the avascular region around the dorsal midline of the developing midbrain. These cells expressed additional macrophage markers such as CD206 and CD11b. Moreover, the CD31⁺F4/80⁺cells phagocytosed apoptotic cells as functionally matured macrophages, adhered to the newly formed subventricular vascular plexus, and then divided into daughter cells. Eventually, these CD31⁺F4/80⁺cells transdifferentiated into NG2/PDGFRβ/desmin-expressing cerebrovascular pericytes, enwrapping and associating with vascular endothelial cells. These data indicate that a subset of cerebrovascular pericytes derive from mature macrophages in the very early phase of CNS vascular development, which in turn are recruited from sites of embryonic hematopoiesis such as the yolk sac by way of blood flow.

Inflammation is implicated in ischemic stroke and is involved in abnormal homeostasis. Activation of the immune system leads to breakdown of the blood–brain barrier and, thereby, infiltration of immune cells into the brain. Upon cerebral ischemia, infiltrated macrophages and microglia (resident CNS immune cell) are activated, change their phenotype to M1 or M2 based on the microenvironment, migrate toward damaged tissue, and are involved in repair or damage. Those of M1 phenotype release pro-inflammatory mediators, which are associated with tissue damage, while those of M2 phenotype release anti-inflammatory mediators, which are related to tissue recovery. Moreover, late inflammation continually stimulates immune cell infiltration and leads to brain infarction. Therefore, regulation of M1/M2 phenotypes under persistent inflammatory conditions after cerebral ischemia is important for brain repair. Herein, we focus on apoptosis signal-regulating kinase 1 (ASK1), which is involved in apoptotic cell death, brain infarction, and production of inflammatory mediators after cerebral ischemia. We hypothesized that ASK1 is involved in the polarization of M1/M2 phenotype and the function of microglia and macrophage during the late stage of ischemia/hypoxia. We investigated the effects of ASK1 in mice subjected to middle cerebral artery occlusion and on BV2 microglia and RAW264.7 macrophage cell lines subjected to oxygen-glucose deprivation. Our results showed that ASK1 silencing effectively reduced Iba-1 or CD11b-positive cells in ischemic areas, suppressed pro-inflammatory cytokines, and increased anti-inflammatory mediator levels at 7 days after cerebral ischemia. In cultured microglia and macrophages, ASK1 inhibition, induced by NQDI-1 drug, decreased the expression and release of M1-associated factors and increased those of M2-associated factors after hypoxia/reperfusion (H/R). At the gene level, ASK1 inhibition suppressed M1-associated genes and augmented M2-associated genes. In gap closure assay, ASK1 inhibition reduced the migration rate of microglia and macrophages after H/R. Taken together, our results provide new information that suggests ASK1 controls the polarization of M1/M2 and the function of microglia and macrophage under sustained-inflammatory conditions. Regulation of persistent inflammation via M1/M2 polarization by ASK1 is a novel strategy for repair after ischemic stroke.

Epidural administration of dexamethasone might reduce postoperative pain in adults. We evaluated whether a caudal block of 0.1 mg kg^–1 dexamethasone combined with ropivacaine improves analgesic efficacy in children undergoing day-case orchiopexy. This randomized, double-blind study included 80 children aged 6 months to 5 yr who underwent day-case, unilateral orchiopexy. Patients received either 1.5 ml kg⁻¹ of 0.15% ropivacaine (Group C) or 1.5 ml kg⁻¹ of 0.15% ropivacaine in which dexamethasone of 0.1 mg kg⁻¹ was mixed (Group D) for caudal analgesia. Postoperative pain scores, rescue analgesic consumption, and side-effects were evaluated 48 h after operation. Postoperative pain scores at 6 and 24 h post-surgery were significantly lower in Group D than in Group C. Furthermore, the number of subjects who remained pain free up to 48 h after operation was significantly greater in Group D [19 of 38 (50%)] than in Group C [four of 37 (10.8%); P<0.001]. The number of subjects who received oral analgesic was significantly lower in Group D [11 of 38 (28.9%)] than in Group C [20 of 37 (54.1%); P=0.027]. Time to first oral analgesic administration after surgery was also significantly longer in Group D than in Group C (P=0.014). Adverse events after surgery including vomiting, fever, wound infection, and wound dehiscence were comparable between the two groups. The addition of dexamethasone 0.1 mg kg⁻¹ to ropivacaine for caudal block can significantly improve analgesic efficacy in children undergoing orchiopexy. NCT01604915.