Bupivacaine hydrochloride (Vivacaine) is a long-acting, amide-type local anesthetic. Bupivacaine hydrochloride reversibly binds to specific sodium ion channels in the neuronal membrane, resulting in a decrease in the voltage-dependent membrane permeability to sodium ions and membrane stabilization; inhibition of depolarization and nerve impulse conduction; and a reversible loss of sensation.

Bupivacaine can induce calcium release from the sarcoplasmic reticulum (SR) in rats and suppress the SR's uptake of calcium.

In vitro, Bupivacaine exhibits cytotoxic effects on bovine articular chondrocytes after an exposure of 15 to 30 minutes. It acts on isolated mitochondria as an uncoupler of oxygen consumption and adenosine diphosphate phosphorylation. Concentration-dependent mitochondrial depolarization and pyridine nucleotide oxidation are induced by Bupivacaine in these isolated mitochondria. Additionally, Bupivacaine triggers the opening of the permeability transition pore (PTP), a cyclosporin A-sensitive inner membrane channel pivotal in various forms of cell death.