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RX BIN: 015558
Group ID: DDN6600
Card Holder ID: DDN6600

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2018 Price of Bupivacaine

Sensorcaine-dextr 0.75% amp



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What is Bupivacaine

A widely used local anesthetic agent.

Bupivacaine mechanism of action

Local anesthetics such as bupivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells, which prevents depolarization. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: (1) pain, (2) temperature, (3) touch, (4) proprioception, and (5) skeletal muscle tone. The analgesic effects of Bupivicaine are thought to potentially be due to its binding to the prostaglandin E2 receptors, subtype EP1 (PGE2EP1), which inhibits the production of prostaglandins, thereby reducing fever, inflammation, and hyperalgesia.

Dosage forms of Bupivacaine

Form Route Strength
Injection infiltration 2.5 mg/mL
Injection infiltration 5 mg/mL
Injection, solution epidural; infiltration; intracaudal 2.5 mg/mL
Prescription Generics


International Brands



()-bupivacaine (RS)-bupivacaine


Hospira, Inc.

CAS number






Affected organisms

Humans and other mammals

Indication of Bupivacaine

For the production of local or regional anesthesia or analgesia for surgery, for oral surgery procedures, for diagnostic and therapeutic procedures, and for obstetrical procedures.

Toxicity of Bupivacaine

The mean seizure dosage of bupivacaine in rhesus monkeys was found to be 4.4 mg/kg with mean arterial plasma concentration of 4.5 mcg/mL. The intravenous and subcutaneous LD 50 in mice is 6 to 8 mg/kg and 38 to 54 mg/kg respectively. Recent clinical data from patients experiencing local anesthetic induced convulsions demonstrated rapid development of hypoxia, hypercarbia, and acidosis with bupivacaine within a minute of the onset of convulsions. These observations suggest that oxygen consumption and carbon dioxide production are greatly increased during local anesthetic convulsions and emphasize the importance of immediate and effective ventilation with oxygen which may avoid cardiac arrest.

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