PubMed · 9526599
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F Engbers. 1997. Propofol opioïd interaction.. https://pubmed.ncbi.nlm.nih.gov/9526599/
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Propofol, the relatively new, short-acting general anesthetic, markedly enhances the action of GABA at the GABAA receptor. To evaluate its effects on field potentials evoked in the dentate gyrus (DG) during the anesthetic and recovery periods, propofol was administered intraperitoneally to behaving rats bearing stimulating electrodes in the dorsal perforant path (DPP), where medial perforant path fibers predominate, and in the anterior piriform cortex (PC; i.e., olfactory cortex), and recording electrodes in the DG. Input from the PC reaches the DG via the lateral perforant path. Population slow waves (SWs) were evoked by paired-pulse stimulation of the PC at a 32 ms interstimulus interval (ISI) to produce paired-pulse facilitation in the awake animal. We had previously demonstrated that amplitude of SW2 (produced by the second stimulus) was greatly decreased by GABAergic drugs and increased by antiGABAergic convulsant agents. After administration of propofol, mean amplitude of SW2 decreased immediately and remained low for 30-60 min during propofol-induced sleep (as expected), then unexpectedly increased to about 1.5- to 2-fold above pretreatment levels at 2-4 h before gradually returning to pretreatment levels. In addition, the DPP was stimulated to produce either paired-pulse inhibition (20 ms ISI) or facilitation (32 ms ISI) of DG population spikes (PSs) in the awake animal. PS2 was much more inhibited during propofol-induced sleep, than during the pretreatment period, consistent with an expected marked increase in recurrent inhibition. An overshoot in PS2 amplitude was observed only occasionally during recovery, suggesting that withdrawal overshoot in amplitudes is more characteristic of PC-evoked DG SW2 potentials. The overshoot in SW2 amplitude during recovery may have been related to propofol's 'rapid on-rapid off' actions on the GABAA receptor, perhaps resulting in a phenomenon like the 'GABA withdrawal syndrome'. Such an effect, if true, may help explain the rare occurrence of seizures, especially during recovery, associated with its use clinically.
BACKGROUND: The purpose of the study was to investigate the potential influence of the anaesthetic agent propofol on immune function in terms of systemic clearance and organ distribution of injected Escherichia coli in a rabbit model. METHODS: Defined numbers of E. coli (1.3 x 10(8) colony-forming units, CFU) were injected intravenously 1 h after starting a 4-h infusion of the anaesthetic propofol (2 ml.kg-1.h-1, Disoprivan 1%; n = 6)) or after saline application (n = 6). As propofol is formulated in a 10% lipid emulsion, the lipid vehicle Intralipid (2 ml.kg-1.h-1; n = 6) alone was investigated in a separate group. Parameters monitored were arterial pressure and rates of bacterial elimination from the blood. Three hours after bacterial injection, the animals were killed, and tissue samples of liver, spleen, lung, and kidney were collected for microbiological examinations. RESULTS: Compared to saline-treated animals, infusion of propofol induced increased accumulation of E. coli in lung and spleen, thus reflecting reticuloendothelial system dysfunction. CONCLUSION: As the lipid emulsion by itself induced the same effects, the impaired immune function due to propofol is thought to be attributed to its solvent Intralipid.
UNLABELLED: Propofol emulsion supports bacterial growth. Extrinsic contamination of propofol has been implicated as an etiological event in postsurgical infections. When added to propofol, local anesthetics (e.g., lidocaine) alleviate the pain associated with injecting it. Because local anesthetics have antimicrobial activity, we determined whether lidocaine would inhibit microbial growth by comparing the growth of four microorganisms in propofol and in mixtures of propofol and lidocaine. Known quanta of Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, and Candida albicans were inoculated into solutions of 1% propofol, 0.2% lidocaine in propofol, 0.5% lidocaine in propofol, 0.5% lidocaine in isotonic sodium chloride solution, and 0.9% isotonic sodium chloride solution. All microorganisms were taken from stock cultures and incubated for 24 h. Growth of microorganisms in each solution was compared by counting the number of colony-forming units grown from a subculture of the solution at 0, 3, 6, 12 and 24 h. Propofol supported the growth of E. coli and C. albicans. Propofol maintained static levels of S. aureus and was bactericidal toward P. aeruginosa. The addition of 0.2% and 0.5% lidocaine to propofol failed to prevent the growth of the studied microorganisms. The effect of 0.5% lidocaine in isotonic sodium chloride solution did not differ from the effects of isotonic sodium chloride solution alone. We conclude that lidocaine, when added to propofol in clinically acceptable concentrations, does not exhibit antimicrobial properties. IMPLICATIONS: Local anesthetics such as lidocaine have antimicrobial activity. Propofol supports the growth of bacteria responsible for infection. Bacteria were added to propofol and propofol mixed with lidocaine. The addition of lidocaine to propofol in clinically relevant concentrations did not prevent the growth of bacteria. The addition of lidocaine to propofol cannot prevent infection from contaminated propofol.