-
Minerva Anestesiologica Sep 2001Ropivacaine is a relatively new long-acting local anesthetic. It is a pure S(-) isomer, with a high pKa and low lipid solubility. Because of its physical and chemical... (Review)
Review
BACKGROUND
Ropivacaine is a relatively new long-acting local anesthetic. It is a pure S(-) isomer, with a high pKa and low lipid solubility. Because of its physical and chemical properties, ropivacaine produces a marked differential in sensory and motor blockades, with a toxic potential lower than other long-acting anesthetic solutions. The purpose of this paper was the evaluation of the literature concerning indications and advantages of ropivacaine for different regional anesthesia techniques.
METHODS
We have evaluated results of prospective, randomized, controlled trials evaluating clinical use of ropivacaine for epidural anesthesia and analgesia, as well as spinal and peripheral nerve blocks.
RESULTS
The literature clearly demonstrates both efficacy and safety of ropivacaine used for epidural anesthesia and analgesia as well as for upper and lower limb peripheral nerve blocks, both single-shot and continuous peripheral blocks. Although ropivacaine has not been registered yet for spinal anesthesia, various studies show its efficacy and safety also in this field. Because of its pharmacodynamic properties, intrathecal ropivacaine seems also interesting for outpatient procedures.
CONCLUSIONS
Ropivacaine is a long-acting local anesthetic with a marked differential blockade between sensory and motor fibres, overall at the low concentrations used for postoperative analgesia. It probably has a slightly lower potency as compared with bupivacaine, but provides similar clinical efficacy in the different fields of regional anesthesia. Ropivacaine is less cardiotoxic and causes less central nervous system toxicity than bupivacaine, and this lower toxic potential has been reported not only with equivalent but also with equipotent concentrations and doses. For this reason, ropivacaine represents a useful alternative to bupivacaine for central and peripheral nerve blocks as well as for the management of postoperative pain relief.
Topics: Amides; Anesthetics, Local; Humans; Ropivacaine
PubMed: 11778088
DOI: No ID Found -
Regional Anesthesia and Pain Medicine Sep 2023
Topics: Humans; Ropivacaine; Anesthetics, Local; Pain, Postoperative
PubMed: 37217259
DOI: 10.1136/rapm-2023-104628 -
Neurotoxicology Dec 2022Due to the increasing use of local anesthetic techniques in various healthcare settings, local anesthetic toxicity still occurs. Seizures are the most common symptom of...
Due to the increasing use of local anesthetic techniques in various healthcare settings, local anesthetic toxicity still occurs. Seizures are the most common symptom of local anesthetic toxicity. The relationship between local anesthetic-induced seizures and the sensation of pain has not been established till now. Here, we assessed the development of pain hypersensitivity after ropivacaine-induced seizures (RIS) and the influence of RIS on incision-induced postsurgical pain and formalin-induced acute inflammatory pain. In addition, the involvement of spinal 5-HT/5-HTR in RIS-induced pain sensitization was investigated. According to a sequential exploratory experimental strategy, we first calculated the 50% seizure dosage of ropivacaine to be 42.66 mg/kg (95% confidence interval: 40.19-45.28 mg/kg). We showed that RIS induced significant bilateral mechanical pain hypersensitivity that lasted around 5 days, accompanied by an increase in spinal 5-HT. Moreover, RIS considerably protracted postsurgical pain and enhanced formalin-induced spontaneous flinching in the second phase. Depletion of spinal 5-HT with intrathecal injection of 5,7-dihydroxytryptamine (5,7-DHT) reduced RIS-induced pain hypersensitivity and prevented the prolonging of postsurgical pain following RIS. Likewise, blocking spinal 5-HT3R by intrathecal administration of ondansetron reversed RIS-induced pain hypersensitivity and attenuated the pronociception of RIS in the formalin test. Our findings revealed that acute RIS led to pain hypersensitivity and had pronociceptive effects on incision-induced postsurgical pain and formalin-induced acute inflammatory pain. Moreover, our data implied that RIS-induced pain sensitization depends on spinal 5-HT/5-HTR signaling. Thus, targeting the descending serotonergic facilitation system should be an important element of the precise treatment for local anesthetic toxicity.
Topics: Rats; Animals; Serotonin; Ropivacaine; Anesthetics, Local; Spinal Cord; Formaldehyde; Pain, Postoperative; Seizures
PubMed: 36209936
DOI: 10.1016/j.neuro.2022.10.001 -
Journal of Nanobiotechnology Dec 2023Chemotherapy can cause severe pain for patients, but there are currently no satisfactory methods of pain relief. Enhancing the efficacy of chemotherapy to reduce the...
Chemotherapy can cause severe pain for patients, but there are currently no satisfactory methods of pain relief. Enhancing the efficacy of chemotherapy to reduce the side effects of high-dose chemotherapeutic drugs remains a major challenge. Moreover, the treatment of chemotherapy-induced peripheral neuropathic pain (CIPNP) is separate from chemotherapy in the clinical setting, causing inconvenience to cancer patients. In view of the many obstacles mentioned above, we developed a strategy to incorporate local anesthetic (LA) into a cisplatin-loaded PF127 hydrogel for painless potentiated chemotherapy. We found that multiple administrations of cisplatin-loaded PF127 hydrogels (PFC) evoked severe CIPNP, which correlated with increased pERK-positive neurons in the dorsal root ganglion (DRG). However, incorporating ropivacaine into the PFC relieved PFC-induced CIPNP for more than ten hours and decreased the number of pERK-positive neurons in the DRG. Moreover, incorporating ropivacaine into the PFC for chemotherapy is found to upregulate major histocompatibility complex class I (MHC-I) expression in tumor cells and promote the infiltration of cytotoxic T lymphocytes (CD8 T cells) in tumors, thereby potentiating chemotherapy efficacy. This study proposes that LA can be used as an immunemodulator to enhance the effectiveness of chemotherapy, providing new ideas for painless cancer treatment.
Topics: Humans; Ropivacaine; Cisplatin; CD8-Positive T-Lymphocytes; Hydrogels; Neuralgia; Antineoplastic Agents
PubMed: 38041074
DOI: 10.1186/s12951-023-02230-5 -
Brazilian Journal of Anesthesiology... 2020Ropivacaine is a long-acting local anesthetic that causes prolonged anesthesia and is beneficial for a wide variety of surgeries. Systemic toxicity has been reported...
INTRODUCTION AND OBJECTIVES
Ropivacaine is a long-acting local anesthetic that causes prolonged anesthesia and is beneficial for a wide variety of surgeries. Systemic toxicity has been reported after usage of high dose ropivacaine or inadvertent intravascular administration. We report a case of ropivacaine withdrawal, which to our knowledge has not been previously described in the literature.
CASE REPORT
The patient presented to our department with uncontrolled belt-like upper-abdominal pain, self-rated as a 9/10 on the numeric rating scale. We decided to use continuous epidural analgesia with ropivacaine through a multi-port epidural catheter. Pain was well controlled for one month without significant adverse effects. However, ropivacaine unexpectedly ran out and two hours later the patient developed agitation, generalized tremor, tachycardia, and tachypnea. These symptoms resolved 30 minutes after reinitiating epidural ropivacaine.
DISCUSSION
Our hypothesis of ropivacaine withdrawal was related to the timing of symptoms in relation to drug administration over two episodes. The possible mechanism of the observed withdrawal syndrome is upregulation of voltage-gated sodium channels after prolonged inhibition, resulting in increase in sodium influx and genetic variation.
Topics: Analgesia, Epidural; Anesthetics, Local; Humans; Male; Middle Aged; Ropivacaine; Substance Withdrawal Syndrome
PubMed: 32173065
DOI: 10.1016/j.bjan.2019.12.006 -
Bioengineered Dec 2021To study whether ropivacaine inhibits the proliferation and migration of colon cancer cells through ITGB1 (Integrin beta-1). First, the effect of ropivacaine on cell...
To study whether ropivacaine inhibits the proliferation and migration of colon cancer cells through ITGB1 (Integrin beta-1). First, the effect of ropivacaine on cell proliferation and migration was detected by MTT and Transwell. DAPI staining, annexin V staining and Western blot were used to detect the expression of apoptosis-related proteins to investigate the effect of ropivacaine on cell apoptosis. Using bioinformatics software to predict the potential drug targets of ropivacaine. RT-PCR, Western blot and immunofluorescence verify the distribution and expression of the drug target ITGB1, and detect its downstream-related proteins to further prove that ropivacaine affects colon cancer cells by acting on ITGB1 protein. 1. Ropivacaine significantly inhibited the proliferation of colon cancer cells and promoted their apoptosis 2. Ropivacaine could interact with ITGB1 protein, and inhibited the expression of ITGB1 protein in colon cancer cells, thereby affecting its downstream signaling pathway. Ropivacaine regulates the function of colon cancer cells by targeting the expression of ITGB1 protein and affecting the activation of its downstream signaling pathways. Integrin beta-1 (ITGB1); 3-(45)-dimethylthiahiazo (-z-y1)-35-di- phenytetrazoliumromide (MTT); 4. 6-diamimo-2-phenyl indole (DAPI); Reverse transcrption PCR (RT-PCR); Colorectal cancer (CRC); Local anesthetics (LA); voltage-gated sodium channel (VGSC); dulbecco s modifed eade medium (DMEM); propidium iodide (PI); dodecyl sulf ate, sodium salt-Polyacrylamide gel electrophoresis (SDS-PAGE); Polyvinylidene Fluoride (PVDF); BCL2 associated X (Bax); Focal Adhesion Kinase (FAK); extracellular signal-regulated kmase (ERK); alpha serme threcnime-proteim kinase (AKT); Glyceraldehyde-3-phosphate dehydrogenase (GAPDH); Tris-buffered salme with 0.1% Tween 20 (TBST); Similarty ensemble approach (SEA).
Topics: Cell Line, Tumor; Cell Movement; Cell Proliferation; Colorectal Neoplasms; HCT116 Cells; Humans; Integrin beta1; Ropivacaine; Signal Transduction
PubMed: 33345684
DOI: 10.1080/21655979.2020.1857120 -
International Journal of Molecular... Feb 2022Breast cancer (BC) is one of the most common types of cancer and the second leading cause of death in women. Local anaesthetics (LAs) and opioids have been shown to... (Review)
Review
Breast cancer (BC) is one of the most common types of cancer and the second leading cause of death in women. Local anaesthetics (LAs) and opioids have been shown to influence cancer progression and metastasis formation in several pre-clinical studies. However, their effects do not seem to promote consensus. A systematic review was conducted using the databases Medline (via PubMed), Scopus, and Web of Science (2010 to December 2021). Search terms included "lidocaine", "ropivacaine", "levobupivacaine", "morphine", "methadone", "breast cancer", "breast carcinoma" and "breast neoplasms" in diverse combinations. The search yielded a total of 784 abstracts for initial review, 23 of which met the inclusion criteria. Here we summarise recent studies on the effect of analgesics and LAs on BC cell lines and animal models and in combination with other treatment regimens. The results suggest that local anaesthetics have anti-tumorigenic properties, hence their clinical application holds therapeutic potential. Regarding morphine, the findings are conflicting, but this opioid appears to be a tumour-promoting agent. Methadone-related results are scarce. Additional research is clearly required to further study the mechanisms underlying the controversial effects of each analgesic or LA to establish the implications upon the outcome and prognosis of BC patients' treatment.
Topics: Anesthetics, Local; Animals; Breast Neoplasms; Cell Line, Tumor; Female; Humans; Levobupivacaine; Lidocaine; Morphine; Ropivacaine; Xenograft Model Antitumor Assays
PubMed: 35163815
DOI: 10.3390/ijms23031894 -
BMC Anesthesiology Sep 2022Ropivacaine is commonly applied for local anesthesia and may cause neurotoxicity. Dexmedetomidine (DEX) exhibits neuroprotective effects on multiple neurological...
BACKGROUND
Ropivacaine is commonly applied for local anesthesia and may cause neurotoxicity. Dexmedetomidine (DEX) exhibits neuroprotective effects on multiple neurological disorders. This study investigated the mechanism of DEX pretreatment in ropivacaine-induced neurotoxicity.
METHODS
Mouse hippocampal neuronal cells (HT22) and human neuroblastoma cells (SH-SY5Y) were treated with 0.5 mM, 1 mM, 2.5 mM, and 5 mM ropivacaine. Then the cells were pretreated with different concentrations of DEX (0.01 μM, 0.1 μM, 1 μM, 10 μM, and 100 μM) before ropivacaine treatment. Proliferative activity of cells, lactate dehydrogenase (LDH) release, and apoptosis rate were measured using CCK-8 assay, LDH detection kit, and flow cytometry, respectively. miR-10b-5p and BDNF expressions were determined using RT-qPCR or Western blot. The binding of miR-10b-5p and BDNF was validated using dual-luciferase assay. Functional rescue experiments were conducted to verify the role of miR-10b-5p and BDNF in the protective mechanism of DEX on ropivacaine-induced neurotoxicity.
RESULTS
Treatment of HT22 or SH-SY5Y cells with ropivacaine led to the increased miR-10b-5p expression (about 1.7 times), decreased BDNF expression (about 2.2 times), reduced cell viability (about 2.5 times), elevated intracellular LDH level (about 2.0-2.5 times), and enhanced apoptosis rate (about 3.0-4.0 times). DEX pretreatment relieved ropivacaine-induced neurotoxicity, as evidenced by enhanced cell viability (about 1.7-2.0 times), reduced LDH release (about 1.7-1.8 times), and suppressed apoptosis rate (about 1.8-1.9 times). DEX pretreatment repressed miR-10b-5p expression (about 2.5 times). miR-10b-5p targeted BDNF. miR-10b-5p overexpression or BDNF silencing reversed the protective effect of DEX pretreatment on ropivacaine-induced neurotoxicity, manifested as reduced cell viability (about 1.3-1.6 times), increased intracellular LDH level (about 1.4-1.7 times), and elevated apoptosis rate (about 1.4-1.6 times).
CONCLUSIONS
DEX pretreatment elevated BDNF expression by reducing miR-10b-5p expression, thereby alleviating ropivacaine-induced neurotoxicity.
Topics: Animals; Apoptosis; Brain-Derived Neurotrophic Factor; Dexmedetomidine; Humans; Lactate Dehydrogenases; Mice; MicroRNAs; Neuroblastoma; Neuroprotective Agents; Ropivacaine
PubMed: 36163004
DOI: 10.1186/s12871-022-01810-6 -
Human & Experimental Toxicology 2022Ovarian cancer is a malignant tumor in women all over the world. Ropivacaine is identified as a potential drug for the treatment of malignant tumors, but the role and...
PURPOSE
Ovarian cancer is a malignant tumor in women all over the world. Ropivacaine is identified as a potential drug for the treatment of malignant tumors, but the role and mechanism of ropivacaine in ovarian cancer remains unknown.
MATERIALS AND METHODS
Ovarian cancer cells were treated with different doses of ropivacaine. The function of ropivacaine in ovarian cancer was assessed using Cell Counting Kit-8 assay, flow cytometry, sphere-formation assay, Western blot, Fe level analysis, and immunofluorescence. Meanwhile, the mechanism of ropivacaine in ovarian cancer was investigated by multiple molecular experiments. The protective function of ropivacaine in ovarian cancer was further confirmed by in vivo assay.
RESULTS
The functional research data indicated that the growth and stemness of ovarian cancer cells were restrained after ropivacaine treatment, while the ferroptosis in ovarian cancer cells was facilitated. The mechanism results confirmed that ropivacaine inactivated the PI3K/AKT signaling pathway in ovarian cancer cells. Furthermore, in vivo assay demonstrated that ropivacaine repressed the proliferation of ovarian cancer cells in vivo and had a protective function in ovarian cancer.
CONCLUSION
Ropivacaine restrained ovarian cancer cell stemness and accelerated cell ferroptosis by inactivating PI3K/AKT signaling pathway.
Topics: Cell Line, Tumor; Cell Proliferation; Female; Ferroptosis; Humans; Ovarian Neoplasms; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Ropivacaine; Signal Transduction
PubMed: 36124980
DOI: 10.1177/09603271221120652 -
International Journal of Nanomedicine 2022Ropivacaine as a conventional local anesthetic has been used more and more frequently in the treatment of postoperative pain, but its analgesic effect can only last for...
INTRODUCTION
Ropivacaine as a conventional local anesthetic has been used more and more frequently in the treatment of postoperative pain, but its analgesic effect can only last for several hours. In order to fulfill the clinic requirement for long-term analgesia, a long-acting ropivacaine nanocrystal formulation was fabricated through the interaction between ropivacaine and a self-assembling peptide.
METHODS
Transmission electron microscopy, dynamic light scattering, circular dichroism and fluorescence spectrometry were used to examine the structural changes caused by the interaction between ropivacaine and the peptide. Scanning electron microscopy, dynamic light scattering, Fourier transform infrared spectrometry, X-ray diffraction and optical microscopy were used to characterize the ropivacaine-peptide nanocrystal. In vitro drug release and pharmacokinetics study were conducted to evaluate the slow-release profile of the nanocrystal formulation. A rodent cutaneous trunci muscle reflex model was used to evaluate the nociceptive blockade effects, and histological analysis was used to evaluate the local toxicity. A rodent plantar incisional pain model was used to evaluate the analgesic effect.
RESULTS
Soluble ropivacaine monomers interacted with the Q11 peptide through π-π stacking and remolded its self-assembling structure, leading to the formation of drug/peptide nanoparticles which could be mineralized to form drug/peptide nanocrystals by adjusting the pH. Under physiological condition, the nanocrystals could release free ropivacaine slowly. As evaluated in rodent models, the anesthetic and analgesic effects of this formulation were significantly extended without causing toxicity.
CONCLUSION
Based on the interaction between ropivacaine and Q11, a controllable biomineralization process could be induced to obtain homogeneous nanocrystals, which could be used as an injectable long-acting analgesic formulation. This crystallization strategy utilizing the peptide-drug interaction also provided a promising pathway to fabricate long-acting formulations for many other small molecular drugs.
Topics: Amides; Analgesia; Anesthetics, Local; Humans; Pain, Postoperative; Peptides; Ropivacaine
PubMed: 35937079
DOI: 10.2147/IJN.S369706