ArticleInternational journal of molecular sciences2025
A Comparative Study of Common Anesthetics Propofol, Sevoflurane, Isoflurane and Ketamine on Lipid Membrane Fluidity.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Interpol review of forensic drug chemistry, 2022-2025.Forensic science international. Synergy · 2026Review
- Fat on Fire: Disrupted Microglial Lipid Metabolism as a Driver of Anesthetic Neurotoxicity.Neuroscience bulletin · 2026Review
- Article
- Shared neuropathological features of mild traumatic brain injury and anesthesia.Frontiers in neurology · 2026Review
- The physiologic power of fluid circulation and implications for fluid therapy.Frontiers in veterinary science · 2026Review
- Isoflurane and Surgical Stress Disrupt Fatty Acid and Carbon Metabolism Leading to Cardiomyopathy.bioRxiv : the preprint server for biology · 2025Article
- Advances in research on propofol-induced postoperative cognitive dysfunction via Piezo channels.Frontiers in molecular neuroscience · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The membrane fluidity increases induced by popular anesthetic agents (propofol, isoflurane, sevoflurane, and ketamine/xylazine) were measured at the clinical and supra-clinical concentrations in red blood cell (RBC) membrane as well as four model membranes. Membrane fluidity changes were monitored using the excimer/monomer (E/M) ratio of dipyrene-PC and fluorescence anisotropies of DPH-PC and TMA-DPH. Propofol, sevoflurane and isoflurane increased membrane fluidity instantaneously. The largest increase occurs in membranes made of saturated lipids. RBCs were labeled with TMA-DPH, and the increase in membrane fluidity at clinical concentrations of isoflurane and sevoflurane was more than that induced by ten times the legal limit of alcohol in human blood. However, membrane fluidity was essentially unchanged by ketamine/xylazine up to 210 µM. These results strongly correlate with our recent in vivo experiments and reveal a clear connection between increasing membrane fluidity in model membranes, increasing the blood-brain barrier (BBB) permeability in mice, and inducing effective anesthesia in animals. Interestingly, at the most commonly used clinical concentrations, the membrane fluidity increases induced by propofol, sevoflurane, and isoflurane were very similar, despite the fact that different categories of anesthetics were used and their chemical concentrations were different by 100 times. This indicates that at clinical concentrations of these anesthetics, a similar level of membrane disruption at the BBB is achieved. Thus, our results strongly support the lipid hypothesis of the mechanism of general anesthetics.
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