Propofol (2,6-diisopropylphenol) is a versatile, short-acting, intravenous (i.v.)
sedative-
hypnotic agent initially marketed as an
anesthetic, and now also widely used for the sedation of patients in the intensive care unit (ICU). At the room temperature
propofol is an oil and is insoluble in water. It has a remarkable safety profile. Its most common side effects are dose-dependent
hypotension and cardiorespiratory depression.
Propofol is a global central nervous system (CNS) depressant. It activates
gamma-aminobutyric acid (
GABA A) receptors directly, inhibits the
N-methyl-d-aspartate (
NMDA) receptor and modulates
calcium influx through slow
calcium-ion channels. Furthermore, at doses that do not produce sedation,
propofol has an
anxiolytic effect. It has also immunomodulatory activity, and may, therefore, diminish the systemic inflammatory response believed to be responsible for organ dysfunction.
Propofol has been reported to have
neuroprotective effects. It reduces cerebral blood flow and intracranial pressure (ICP), is a potent
antioxidant, and has anti-inflammatory properties. Laboratory investigations revealed that it might also protect brain from ischemic injury.
Propofol formulations contain either disodium edetate (
EDTA) or
sodium metabisulfite, which have antibacterial and antifungal properties.
EDTA is also a
chelator of divalent
ions such as
calcium,
magnesium, and
zinc. Recently,
EDTA has been reported to exert a
neuroprotective effect itself by chelating surplus intracerebral
zinc in an
ischemia model. This article reviews the
neuroprotective effects of
propofol and its mechanism of action.