期刊
ANESTHESIOLOGY
卷 101, 期 3, 页码 703-709出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00000542-200409000-00019
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资金
- NIGMS NIH HHS [GM55876] Funding Source: Medline
Background: The majority of surgical patients receive inhaled anesthetics, principally small haloalkanes and haloethers. Long-term cognitive problems occur in the elderly subsequent to anesthesia and surgery, and previous surgery might also be a risk factor for neurodegenerative disorders like Alzheimer and Parkinson disease. The authors hypothesize that inhaled anesthetics contribute to these effects through a durable enhancement of peptide oligomerization. Methods: Light scattering, filtration assays, electron microscopy, fluorescence spectroscopy and size-exclusion chromatography was used to characterize the concentration-dependent effects of halothane, isoflurane, propofol, and ethanol on amyloid beta peptide oligomerization. Pheochromocytoma. cells were used to characterize cytotoxicity of amyloid oligomers with and without the above anesthetics. Results: Halothane and isoflurane enhanced amyloid beta oligomerization rates and pheochromocytoma cytotoxicity in vitro through a preference for binding small oligomeric species. Ethanol and propofol inhibited oligomerization at low concentration but enhanced modestly at very high concentration. Neither ethanol nor propofol enhanced amyloid 0 toxicity in pheochromocytoma cells. Conclusions: Inhaled anesthetics enhance oligomerization and cytotoxicity of Alzheimer disease-associated peptides. In addition to the possibility of a general mechanism for anesthetic neurotoxicity, these results call for further evaluation of the interaction between neurodegencrative disorders, dementia, and inhalational anesthesia.
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