|Place of Origin:||CHINA|
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|Minimum Order Quantity:||10g|
|Packaging Details:||Disguised Package|
|Delivery Time:||2 Working Days|
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|Supply Ability:||100 KG/Month|
|Appearance:||White Powder||Usage:||Local Anesthetic|
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Levobupivacaine is a local anaesthetic drug belonging to the amino amide group. It is the S-enantiomer of bupivacaine. Levobupivacaine hydrochloride is commonly marketed by Abbott under the trade name Chirocaine. Bupivacaine is an amide-type local anaesthetic. Although it blocks neuro transmission, its membrane stabilising action also affects the myocardium. This can cause fatal cardiotoxicity. As bupivacaine is widely used in surgery and obstetrics, attempts have been made to develop a safer long-acting local anaesthetic.
The bupivacaine molecule is a racemic compound. Levobupivacaine is the S-enantiomer of bupivacaine and is thought to have less cardiotoxic potential than the R-enantiomer. The pharmacokinetic parameters of levobupivacaine are similar to those of bupivacaine.
Levobupivacaine has been studied in surgical anaesthesia and for pain management. It can be used for local infiltration, epidural, intrathecal and peripheral nerve blocks. For epidural analgesia it can be given with clonidine. Double-blind comparisons of levobupivacaine and bupivacaine show that their anaesthetic effects are similar.
Levobupivacaine is a long acting, amide-type local anaesthetic that is the S(−) 3- isomer of the racemate bupivacaine. In general, in vitro, in vivo and human volunteer studies of nerve block indicate that levobupivacaine is as potent as bupivacaine and produces similar sensory and motor block. A trend towards a longer sensory block with levobupivacaine was seen in some studies, and may be related to the greater vasoconstrictive activity of levobupivacaine than that of the R(+)-enantiomer (dexbupivacaine) at lower doses. The minimum local analgesic concentration was 0.083% for epidural levobupivacaine 20ml and 0.081% for bupivacaine 20ml in women in the first stage of labour.
A lower risk of CNS toxicity with levobupivacaine compared with dexbupivacaine and/or bupivacaine has also been reported, including less propensity to cause apnoea and higher convulsive doses (levobupivacaine 103mg vs bupivacaine 85mg) in animal studies. In human volunteers, 64% of intravenous bupivacaine recipients (mean dose 65.5mg) compared with 36% of levobupivacaine (67.7mg) recipients experienced central or peripheral nervous system disorders. Intravenous levobupivacaine 40mg produced fewer changes indicative of CNS depression on EEG than bupivacaine 40mg in volunteers.
When compared with ropivacaine in animals, levobupivacaine had similar or more pronounced nerve blocking effects, depending on the concentration and model. Levobupivacaine and ropivacaine had generally similar cardiovascular effects in in vitro and animal studies, although some studies reported greater QRS interval prolongation and/or arrhythmogenic risk with levobupivacaine at some concentrations, but no difference in mortality rates. However, cardiotoxicity has not been compared at established equipotent anaesthetic doses.
Only limited pharmacokinetic data are available for levobupivacaine. The plasma concentrations of levobupivacaine are dependent on dose and route of administration. Maximum plasma concentrations were 0.58 to 1.02 mg/L after epidural administration of 75 to 150mg, and 0.47 and 0.96 mg/L after brachial plexus block with 1 and 2 mg/kg, respectively, in patients. The elimination half-life after intravenous administration of 40mg in volunteers was 1.3 hours and the volume of distribution was 67L. Levobupivacaine is highly protein bound (>97%). The drug is extensively metabolised by the cytochrome P450 (CYP) system, primarily CYP1A2 and CYP3A4 isoforms, and then excreted in the urine (71% within 48 hours) and faeces (24%).
Levobupivacaine crosses the placenta, with an umbilical vein/maternal vein drug concentration ratio of 0.3 after epidural levobupivacaine 0.5% (150mg) in women undergoing Caesarean section.
After administration of racemic bupivacaine, it appears that systemic disposition is enantioselective, particularly with regards to plasma protein binding, which is higher with levobupivacaine than dexbupivacaine. Levobupivacaine does not undergo racaemisation in vivo.
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|Anesthetic (Raw Powder)|