Anesth Analg 2007; 105:1863-1864
© 2007 International Anesthesia Research Society
doi: 10.1213/01.ane.0000287633.64654.64
LETTER TO THE EDITOR
Section Editor:
Lawrence Saidman
When Lack of Addition Really Does Add Up
Hong Liu, MD
Associate Professor; Department of Anesthesiology and Pain Medicine; University of California Davis Health System; Sacramento, California; hualiu{at}ucdavis.edu
In Response:
Dr. Pagel (1) raises an issue worth both discussion and further exploration regarding the actions and possible interactions of lower concentrations of inhalational anesthetic agents with pre- and postconditioning. The studies referenced in his comments differ from ours in many aspects. They combine inhalational anesthetic preconditioning with ischemic postconditioning, delayed preconditioning with postconditioning, or prolonged and multiple episodes of preconditioning. In addition, they are in vivo experiments. In contrast, our study uses sevoflurane alone to provide both acute preconditioning and postcondtioning in an in vitro model (2).
The studies presented do suggest the possibility of additive effects of combined preconditioning and postcondtioning compared with any of the preconditioning or postconditioning triggers alone. As we discussed in our manuscript, there is no doubt that different results could be due to differences in experimental design. For example, the mechanisms for ischemic preconditioning may be very different from those involved in anesthetic preconditioning. Sergeev et al. studied the changes in gene expression with anesthetic and ischemic preconditioning and reported only a very small percentage of overlap in the multiple up and down regulated genes (3). It has also been proposed that the mechanisms of acute preconditioning differ from delayed (second window) preconditioning. Acute preconditioning involves primarily posttranslational modifications, whereas delayed precondtioning also involves modified gene expression and synthesis of cardioprotective proteins (4). Even the use of different anesthetic agents could contribute to different results. Isoflurane has been reported not to produce a delayed preconditioning (5).
In our discussion, we suggested that exposure to higher concentrations of sevoflurane could produce different results. We would also agree with Dr. Pagel that lower concentrations of sevoflurane might produce different results. Comprehensive dose response studies of anesthetic pre- and postconditioning in an in vitro model would be a constructive addition to this area of research.
REFERENCES
- Pagel PS. When lack of addition really does addup. Anesth Analg 2007;105:1863[Free Full Text]
- Deyhimy DI, Fleming NW, Brodkin IG, Liu H. Anesthetic preconditioning combined with postconditioning offers no additional benefit over preconditioning or postconditioning alone. Anesth Analg 2007;105:316–24[Abstract/Free Full Text]
- Sergeev P, da Silva R, Lucchinetti E, Zaugg K, Pasch T, Schaub MC, Zaugg M. Trigger-dependent gene expression profiles in cardiac preconditioning. Anesthesiology 2004;100:474–88[Web of Science][Medline]
- Baines CP, Pass JM, Ping P. Protein kinase-modulated effectors in the late phase of ischemic preconditioning. Basic Res Cardiol 2001;96:207–18[Web of Science][Medline]
- Kehl F, Pagel PS, Krolikowski JG, Gu W, Toller W, Warltier DC, Kersten JR. Isoflurane does not produce a second window of preconditioning against myocardial infarction in vivo. Anesth Analg 2002;95: 1162–8[Abstract/Free Full Text]
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