Effect of hypercarbia and isoflurane on brain cell death and neurocognitive dysfunction in 7-day-old rats
| Autor: | Michael T. Lee, Emanuel J. Zusmer, Rehan S. Alvi, Jeffrey W. Sall, Vinuta Rau, Ban Ku, Joan F. Hilton, Laura D. V. May, Kavel Visrodia, Atoosa Firouzian, Ran Dai, Brandi K. Ormerod, Joseph S. Bell, Jeremy N. Guggenheim, Greg Stratmann |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Male
Minimum alveolar concentration Time Factors Cell Survival Spatial memory Rats Sprague-Dawley Conditioning Psychological Medicine Animals Fear conditioning Cell Proliferation Neurons Memory Disorders Dose-Response Relationship Drug Isoflurane business.industry Working memory Cognitive disorder Cell Differentiation Fear Carbon Dioxide medicine.disease Rats Survival Rate Anesthesiology and Pain Medicine Treatment Outcome Anesthesia Anesthetic Anesthetics Inhalation Female Blood Gas Analysis business Neurocognitive medicine.drug |
| Zdroj: | Anesthesiology. 110(4) |
| ISSN: | 1528-1175 |
| Popis: | Background: Millions of neonates undergo anesthesia each year. Certain anesthetic agents cause brain cell death and longterm neurocognitive dysfunction in postnatal day (P)7 rats. Despite its intuitive appeal, a causal link between cell death and neurocognitive decline after anesthesia has not been established. If one existed, the degree of cell death would be expected to correlate with the degree of neurocognitive dysfunction caused by anesthesia. The authors therefore tested if cell death caused by various durations of isoflurane at 1 minimum alveolar concentration causes duration-dependent long-term neurocognitive dysfunction. Methods: Isoflurane was administered to P7 rats at 1 minimum alveolar concentration for 0, 1, 2, or 4 h. To control for the respiratory depressant effects of anesthesia, a group of rats was treated wit h4ho fcarbon dioxide. Cell death was assessed by FluoroJade staining 12 h after the end of each intervention, and neurocognitive outcome was assessed 8 weeks later by using fear conditioning, spatial reference memory, and spatial working memory tasks. Results: Widespread brain cell death was caused b y2ha nd 4 h of isoflurane and b y4ho fcarbon dioxide. The degree and distribution of thalamic cell death was similar in 4 h isofluranetreated and 4-h carbon dioxide‐treated rats. Onl y4ho fisoflurane caused a long-term neurocognitive deficit affecting both spatial reference memory and spatial working memory. Working memory was improved in carbon dioxide‐treated rats. Conclusion: Isoflurane-induced brain cell death may be partly caused by hypercarbia. The inconsistencies between cell death and neurocognitive outcome suggest that additional or alternative mechanisms may mediate anesthesia-induced longterm neurocognitive dysfunction. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|