Use of a curved needle to facilitate four-in-one nerve block performance after total knee arthroplasty in elderly patients: a randomized clinical trial.

Background: Peripheral nerve block is the main analgesic technique for total knee arthroplasty (TKA) in elderly patients. Accurate delivery of the needle tip to the target nerve under ultrasound-guided is a prerequisite for successful nerve block. Failed needle-tip positioning in sciatic nerve (SN) or medial femoral cutaneous nerve (MFCN) block can be due to anatomical structure shadow.

Ultrasound-guided internal branch of superior laryngeal nerve block on postoperative sore throat: A randomized controlled trial.

Introduction: Ultrasound-guided internal branch of the upper laryngeal nerve block (USG-guided iSLN block) have been used to decrease the perioperative stress response of intubation. It is more likely to be successful than blindly administered superior laryngeal nerve blocks with fewer complications. Here, we evaluated the efficacy of USG-guided iSLN block to treat postoperative sore throat (postoperative sore throat, POST) after extubation.

Muscone reduced the hypnotic and analgesic effect of ketamine in mice.

Background: The aim of this study was to determine the effects of different concentrations of muscone on the ketamine requirement for hypnosis and analgesia and possible mechanism in mice.

Methods: In the hypnotic response experiment, muscone (0.5, 1.

Sevoflurane Protects against Intestinal Ischemia-Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma/Nuclear Factor-κB Pathway in Rats.

Background: Intestinal ischemia/reperfusion (I/R) injury is a clinical challenge with high morbidity and mortality, whereas the effective therapeutic strategy is limited. Inflammatory reaction plays important roles in I/R-induced intestinal damage and multi-organ dysfunction syndrome. Peroxisome proliferator-activated receptor gamma (PPARγ) has been identified as an endogenous anti-inflammatory regulator by inhibiting nuclear factor-κB (NF-κB) activation.

Ligustrazine Enhances the Hypnotic and Analgesic Effect of Ketamine in Mice.

The purpose of this study was to determine the effects of different concentrations of ligustrazine, an extract from Chinese herb, on ketamine requirement for hypnosis and analgesia in mice. In the hypnotic response study, mice were randomly allocated to receive saline or ligustrazine at 10, 20, 40, 80 or 160 mg·kg by intraperitoneal injection. Ketamine was administrated 15 min after ligustrazine injection.

Influence of sevoflurane exposure on mitogen-activated protein kinases and Akt/GSK-3β/CRMP-2 signaling pathways in the developing rat brain.

Prolonged exposure to volatile anesthetics causes neurodegeneration in developing animal brains. However, their underlying mechanisms of action remain unclear. The current study investigated the expression of proteins associated with the mitogen-activated protein kinases (MAPK) and protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β)/collapsin response mediator protein 2 (CRMP-2) signaling pathways in the cortices of neonatal mice following exposure to sevoflurane.

Calpain and JNK pathways participate in isoflurane - induced nucleus translocation of apoptosis-inducing factor in the brain of neonatal rats.

Recent studies have demonstrated that volatile anesthetic causes caspase-dependent neuroapoptosis and persistent cognitive deficits in young animals. Apoptosis-inducing factor (AIF) can trigger apoptosis by caspase-independent pathway. Whether isoflurane induces neuroapoptosis by activation of AIF and its possible mechanism are underdetermined.

Sevoflurane Preconditioning Reduces Intestinal Ischemia-Reperfusion Injury: Role of Protein Kinase C and Mitochondrial ATP-Sensitive Potassium Channel.

Ischemic preconditioning (IPC) has been considered to be a potential therapy to reduce ischemia-reperfusion injury (IRI) since the 1980s. Our previous study indicated that sevoflurane preconditioning (SPC) also reduced intestinal IRI in rats. However, whether the protective effect of SPC is similar to IPC and the mechanisms of SPC are unclear.

Sevoflurane protects against intestinal ischemia-reperfusion injury partly by phosphatidylinositol 3 kinases/Akt pathway in rats.

Background: Intestinal ischemia-reperfusion injury (IRI) is a clinical challenge with high morbidity and mortality, leading to intestine damage, systemic inflammation, and multiorgan failure. Previous research has shown that the inhaled anesthetic sevoflurane protects various organs from IRI. However, whether sevoflurane protects against intestinal IRI and which application condition is the most effective are not completely clear.

Both JNK and P38 MAPK pathways participate in the protection by dexmedetomidine against isoflurane-induced neuroapoptosis in the hippocampus of neonatal rats.

Dexmedetomidine, a highly selective α2-adrenergic agonist, has been reported to attenuate isoflurane-induced cognitive impairment and neuroapoptosis. However, the underlying molecular mechanisms remain poorly understood. The aim of this study was to investigate whether mitogen-activated protein kinase (MAPK) pathway was involved in dexmedetomidine-induced neuroprotection against isoflurane effects.

Dexmedetomidine reduces isoflurane-induced neuroapoptosis partly by preserving PI3K/Akt pathway in the hippocampus of neonatal rats.

Prolonged exposure to volatile anesthetics, such as isoflurane and sevoflurane, causes neurodegeneration in the developing animal brains. Recent studies showed that dexmedetomidine, a selective α2-adrenergic agonist, reduced isoflurane-induced cognitive impairment and neuroapoptosis. However, the mechanisms for the effect are not completely clear.

JNK pathway may be involved in isoflurane-induced apoptosis in the hippocampi of neonatal rats.

Previous studies have demonstrated that isoflurane, a commonly used volatile anesthetic, can induce widespread apoptosis in the neonatal animal brains and result in persistent cognitive impairment. Isoflurane-induced cytosolic Ca(2+) overload and activation of mitochondrial pathway of apoptosis may be involved in this neurodegeneration. The c-Jun N-terminal kinase (JNK) signaling can regulate the expression of the Bcl-2 family members that modulates mitochondrial membrane integrity.

Brain and behavior changes in 12-month-old Tg2576 and nontransgenic mice exposed to anesthetics.

Inhaled anesthetics have been shown to increase the aggregation of amyloid beta in vitro through the stabilization of intermediate toxic oligomers, which are thought to contribute to neurocognitive dysfunction in Alzheimer's disease. Inhaled anesthetics may escalate cognitive dysfunction through enhancement of these intermediate oligomer concentrations. We intermittently exposed 12-month-old Tg2576 transgenic mice and nontransgenic littermates to isoflurane and halothane for 5 days.

Ginkgo biloba extract (EGb 761) attenuates lung injury induced by intestinal ischemia/reperfusion in rats: roles of oxidative stress and nitric oxide.

Aim: To investigate the effect of ginkgo biloba extract (EGb 761) on lung injury induced by intestinal ischemia/reperfusion (II/R).

Methods: The rat model of II/R injury was produced by clamping the superior mesenteric artery for 60 min followed by reperfusion for 180 min. The rats were randomly allocated into sham, II/R, and EGb + II/R groups.