Bupivacaine Hydrochloride - CAS 14252-80-3
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Bupivacaine Hydrochloride
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CAS 14252-80-3 Bupivacaine Hydrochloride

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CAS 14252-80-3 Bupivacaine Hydrochloride

Bupivacaine Hydrochloride
(CAS: 14252-80-3)

Reference Reading

1. Degeneration and regeneration of neuromuscular junction architecture in rat skeletal muscle fibers damaged by bupivacaine hydrochloride
TOMIE NISHIZAWA, HIROYUKI TAMAKI, NORIKATSU KASUGA and HIROAKI TAKEKURA,* Journal of Muscle Research and Cell Motility 24: 527–537, 2003.
Many local anaesthetic agents are known to damage skeletal muscle fibers and cause functional deficiencies (Benoit and Belt, 1970; Duchen et al., 1974; Jones, 1982; Nonaka et al., 1983; Tomas I Ferre et al., 1989; Louboutin et al., 1996; Komai and Lokuta, 1999). Bupivacaine hydrochloride (1-n-butyl-DL-piperidine-2-carboxylic acid-2,6-dimethyl anilide hydrochloride: BPVC) causes acute muscle fiber necrosis and massive cellular infiltration of macrophages, followed by rapid regeneration of muscle fibers. Muscle fibers respond to the insults not only by degenerating but also by regenerating in a remarkably complete way (Benoit and Belt, 1970). Physiological and histopathological evidence also supports the idea that muscle regeneration follows the steps of normal myogenesis (Louboutin et al.,1996). In contrast to the muscle damage caused by various grafting procedures, BPVC does not damage satellite cells (Hall-Craggs, 1980a; Hall-Graggs, 1980b), the vasculature (Grim et al., 1983), basal lamina, endomysial tubes (Hall-Graggs, 1974), nor intramuscular nerves (Tomas I Ferre et al., 1989).
2. Bupivacaine Hydrochloride Induces Muscle Fiber Necrosis and Hydroxyl Radical Formation-Dimethyl Sulphoxide Reduces Hydroxyl Radical Formation
Nobuo Wakata, Hideki Sugimoto. Neurochemical Research, Vol. 26, No. 7, July 2001 (©2001), pp. 841–844
A number of studies of free radicals in skeletal muscle were performed in the 1980s, however, after the discovery of dystrophine, the number sharply declined. Even after the discovery of dystrophine an effective treatment for muscular dystrophy has yet to be found. In 1998, Rando et al. reported that oxidative damage might be the primary pathogenetic process responsible for muscular dystrophy. We were encouraged by this report to study free radical formation in the necrotic muscle, and modified our methods for studying hydroxyl radical formation in the brain to investigate therapeutic drugs for conditions involving muscle necrosis, such as myopathy. The local anesthetic bupivacaine hydrochloride (BPVC) causes preferential damage to muscle fibers resulting in massive myonecrosis followed by a rapid repair process, conditions quite similar to those observed in Duchenne muscular dystrophy. We exam- ined whether dimethyl sulphoxide (DMSO) could reduce BPVC-induced hydroxyl radical formation by measuring dihydroxybenzoic acid (DHBA) with the salicylate-trapping method.
3. In Vitro and In Vivo Drug Release from a Novel In Situ Forming Drug Delivery System
Heiko Kranz, Erol Yilmaz, Gayle A. Brazeau, and Roland Bodmeier. Pharmaceutical Research, Vol. 25, No. 6, June 2008
Local anesthetic blockade of nerves is a mainstay in the management of many forms of acute and chronic pain. Following a single injection, currently available local anesthetics rarely provide analgesia for longer than 4–6 h.Infusion pumps with indwelling catheters are possible alternatives. However, these catheter infusions are awkward or difficult to secure in many locations in the body. Nerve blocks with phenol, alcohol, heat, or cryoprobes produce localized tissue destruction, unwanted deficits, and new forms of pain. Application of a timed-release local anesthetic preparation adjacent to nerves was shown to provide prolonged regional anesthesia of peripheral nerves in patients with postoperative pain, cancer, nerve injuries, chronic orofacial pain, or other conditions requiring chronic pain management. In general, the regional administration of local anesthetic drugs should be improved by the development of a drug delivery system leading to sustained release of the drug at the site of application while reducing systemic drug levels. This is particularly important with the highly potent but cardiovascular toxic bupivacaine hydrochloride.
4. Topical bupivacaine compared to bupivacaine infiltration for post‑tonsillectomy pain relief in children: a prospective randomized controlled clinical study
Mehmet Haksever • Süay Özmen • Davut Akduman • Fevzi Solmaz. Eur Arch Otorhinolaryngol (2014) 271:2555–2559
There were no differences in mean age, body mass index, sex distribution, tonsillectomy indication and intraoperative bleeding volume between the three groups (p > 0.05) (Table 1). The post-operative pain scores at 1 h were similar among the groups (p > 0.05). Pain scores in topical bupivacaine hydrochloride group were significantly lesser than the topical saline group at 5th, 13th, 17th and 21st hour, until the 6th day (p < 0.017). Moreover, pain scores of topical bupivacaine hydrochloride group were superior to bupivacaine hydrochloride infiltration group at 5th, 13th, 17th hour and 2nd, 3rd, 4th and 5th day (p < 0.017). Pain scores of bupivacaine hydrochloride infiltration were lesser than saline group at 17th, 21st hour and 1st, 2nd, 3rd, 4th, 5th and 6th day (p < 0.017) whereas, there was no significant difference at other times (Table 2).