Figure 22.5 • Metabolism of propofol.
manufacturer's instructions to prevent microbial contamination and possible sepsis.
Although unrelated chemically to the inhaled anesthetics, propofol has been shown to be a positive modulator of the GABAA receptor. The binding site on GABAA is distinct from the benzodiazepine binding site, and propofol binding is not inhibited by the benzodiazepine antagonist flumazenil.41 The propofol binding site is believed to be on the 3 subunit. Propofol also directly activates Cl currents at glycine receptors, the predominant spinal inhibitory receptor. Unlike many volatile general anesthetics, propofol does not enhance the function of serotonin 5-HT3 receptors and this may explain its low incidence of postoperative nausea and vomiting.42 Propofol shows no analgesic properties, but it does not increase sensitivity to pain like some barbi-turates.43 Propofol causes a dose-dependent decrease in blood pressure and heart rate and a threefold to fourfold increase in serum triglyceride concentrations after 7 days of administration.40
Propofol is quickly and extensively metabolized with 88% of a 14C-labelled intravenous administered dose appearing in the urine as conjugates. Less than 2% of the dose is found unchanged in the feces and less than 0.3% found unchanged in the urine (Fig 22.5). Thirty minutes after the 14C-labelled dose was administered, 81% of the radioactivity was in the form of metabolites.43 Propofol has a quick onset of action (arm-to-brain circulation time) and a quick recovery time.
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