Objective To investigate the influence of sufentanial in postoperative patient controlled epidural analgesia(PCEA) in hemorheology after total hip replacement and its inhibitory effect on thrombosis.Methods Fifty patients,ASA Ⅰ-Ⅱ,undergone total hip replacement were randomly divided into PCEA group (n=25) and control group (n=25), and received continuous epidural anesthesia.After operation,5 mL 0.2% ropivacaine was administered in PCEA group,and then PCEA pump was used,analgesia liquid included 0.4 mg·L-1 sufentanial,0.2% ropivacaine and saline.Petidine was administered intramuscuarly according to pain in control group.VAS scores 1,12,24 and 48 h after operation and changes of various parameters of hemorheology at diffenent time after anesthesia were observed.Results ①The VAS scores 1,12,24,48 h after operation were lower than those in control group (P0.05).②The plasma viscolities and fibrinogen levels in two groups 1 h after anesthesia and at the end of operation were significantly lower than before anesthesia (P0.05);48 h after operation,they were higher in control group than those in PCEA group(P0.05).The viscosity shear rates of whole blood in two groups 1 h after anesthesia and at the end of operation were lower than before anesthesia(P0.05).Conclusion Sufentanial in PCEA can improve the hemorheological parameters after total hip replacement and can be used as a effective method to reduce thrombosis.
ABSTRACT Alantolactone, a sesquiterpene lactone compound, has variety of pharmacological properties, including anti‐inflammatory and antineoplastic effects. In our study, alantolactone inhibited cancer cell proliferation. To explore the mechanisms underlying its antitumor action, we further examined apoptotic cells and cell cycle distribution using flow cytometry analysis. Alantolactone triggered apoptosis and induced cell cycle G1/G0 phase arrest. Furthermore, the expressions of caspases‐8, ‐9, ‐3, PARP, and Bax were significantly upregulated, while antiapoptotic factor Bcl‐2 expression was inhibited. In addition, the expressions of cyclin‐dependent kinase 4 (CDK4), CDK6, cyclin D3, and cyclin D1 were downregulated by alantolactone. Therefore, our findings indicated that alantolactone has an antiproliferative role on lung squamous cancer cells, and it may be a promising chemotherapeutic agent for squamous lung cancer SK‐MES‐1 cells.
From a clinical perspective, local anesthetics have rather widespread application in regional blockade for surgery, postoperative analgesia, acute/chronic pain control, and even cancer treatments. However, a number of disadvantages are associated with traditional local anesthetic agents as well as routine drug delivery administration ways, such as neurotoxicity, short half-time, and non-sustained release, thereby limiting their application in clinical practice. Successful characterization of drug delivery systems (DDSs) for individual local anesthetic agents can support to achieve more efficient drug release and prolonged duration of action with reduced systemic toxicity. Different types of DDSs involving various carriers have been examined, including micromaterials, nanomaterials, and cyclodextrin. Among them, nanotechnology-based delivery approaches have significantly developed in the last decade due to the low systemic toxicity and the greater efficacy of non-conventional local anesthetics. Multiple nanosized materials, including polymeric, lipid (solid lipid nanoparticles, nanostructured lipid carriers, and nanoemulsions), metallic, inorganic non-metallic, and hybrid nanoparticles, offer a safe, localized, and long-acting solution for pain management and tumor therapy. This review provides a brief synopsis of different nano-based DDSs for local anesthetics with variable sizes and structural morphology, such as nanocapsules and nanospheres. Recent original research utilizing nanotechnology-based delivery systems is particularly discussed, and the progress and strengths of these DDSs are highlighted. A specific focus of this review is the comparison of various nano-based DDSs for local anesthetics, which can offer additional indications for their further improvement. All in all, nano-based DDSs with unique advantages provide a novel direction for the development of safer and more effective local anesthetic formulations.
Abstract Objectives The erector spinae plane (ESP) block is a newly defined regional anesthesia technique first described in 2016. The aim of this meta-analysis is to assess the efficacy of ESP block in improving analgesia following lumbar surgery. Methods PubMed, EMBASE, Cochrane Library, and Web of Science were searched for randomized controlled trials (RCTs) that compared the analgesic efficacy of the ESP block with non-block care for lumbar surgery from inception 3 August 2021. The primary outcomes were postoperative opioid consumption and pain scores during the first 24 h. Postoperative pain was measured as pain at rest and on movement at postoperative 0, 4, 8, 12, and 24 h expressed on a visual analog scale (VAS), where 0 = no pain and 10 = the most severe pain. Results 11 studies involving 775 patients were included in our analysis. The use of ESP block significantly decreased 24-h opioid consumption (WMD, -8.70; 95% CI, -10.48 to -6.93; I 2 = 97.5%; P < 0.001) compared with the non-block. Moreover, ESP block reduced pain scores at postoperative time-points up to 24 h. ESP block also prolonged the time to first analgesic request (WMD = 6.93; 95% CI: 3.44 to 10.43, I 2 = 99.8%; P < 0.001). There was less PONV with ESP block versus non-block group (RR, 0.354; 95% CI, 0.23 to 0.56; I 2 = 25.2%; P < 0.001), but no difference in pruritus. Conclusions ESP block provides less opioid consumption and PONV, lower pain scores, and longer time to first analgesic request in patients undergoing lumbar surgery compared to general anesthesia alone.
Exercise-related transient abdominal pain (ETAP) is an ailment commonly known to athletes as stitch and detrimental to their performance although it is thought of as benign and self-limiting. It may be stabbing or sharp when severe, aching, pulling or cramping when less intense, recurrent, and resistant to treatment. To date, ETAP remains under analyzed and under reported in the medical literature. There is no direct evidence of the cause of this ailment. Most of the patients reported in the previous literature were adult patients. This case report of an 11- year-old otherwise healthy female and subsequent analysis of literature, will present a contemporary understanding of ETAP, including the various ideas about the etiology, the epidemiology associated with it, and strategies to manage and prevent this frustrating disorder.
Given that the incidence of cancer is dramatically increasing nowadays, cancer-related neuropathic pain including tumor-related and therapy-related pain gradually attracts more attention from researchers, which basically behaves as a metabolic-neuro-immune disorder with worse clinical outcomes and prognosis. Among various mechanisms of neuropathic pain, the common underlying one is the activation of inflammatory responses around the injured or affected nerve(s). Innate and adaptive immune reactions following nerve injury together contribute to the regulation of pain. On the other hand, the tumor immune microenvironment involving immune cells, as exemplified by lymphocytes, macrophages, neutrophils and dendritic cells, inflammatory mediators as well as tumor metastasis have added additional characteristics for studying the initiation and maintenance of cancer-related neuropathic pain. Of interest, these immune cells in tumor microenvironment exert potent functions in promoting neuropathic pain through different signaling pathways. To this end, this review mainly focuses on the contribution of different types of immune cells to cancer-related neuropathic pain, aims to provide a comprehensive summary of how these immune cells derived from the certain tumor microenvironment participate in the pathogenesis of neuropathic pain. Furthermore, the clarification of roles of various immune cells in different tumor immune microenvironments associated with certain cancers under neuropathic pain states constitutes innovative biology that takes the pain field in a different direction, and thereby provides more opportunities for novel approaches for the prevention and treatment of cancer-related neuropathic pain.
Neural plasticity, a fundamental mechanism of neuronal adaptation, is disrupted in depression. The changes in neural plasticity induced by stress and other negative stimuli play a significant role in the onset and development of depression. Antidepressant treatments have also been found to exert their antidepressant effects through regulatory effects on neural plasticity. However, the detailed mechanisms of neural plasticity in depression still remain unclear. Therefore, in this review, we summarize the recent literature to elaborate the possible mechanistic role of neural plasticity in depression. Taken together, these findings may pave the way for future progress in neural plasticity studies.
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