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Volatile anesthetics not only induce anesthesia, but also render organs resistant against ischemic damage. For example, the magnitude of an experimentally induced myocardial infarct size can be reduced by more than 50% by the administration of volatile anesthetics, even if the administration has been discontinued prior to the ischemic injury (anesthetic-induced preconditioning, APC). Recently, it has been described that volatile anesthetics also exert cardioprotective properties when administered after the ischemic injury (anesthetic-induced postconditioning, APOST). This might be of enormous therapeutical implications since myocardial ischemia is often unpredictable. These protective effects are also effective in other organ systems; e.g. the brain. APC is as effective as ischemic preconditioning and thus represents one of the most potent therapeutic strategies of infarct size reduction. Surgery-related temporary ischemia of the heart or the brain can be prevented using APC in the perioperative period.
However, infarct sparing therapies can often only be applied after the patient’s admission to the hospital. Even in this situation the patient can benefit from the application of volatile anesthetics: volatile anesthetics reduce myocardial infarct size even when they are administered as late as during reperfusion of the occluded vessel (postconditioning).
The intracellular mechanisms underlying APC are under intense investigation. The projects performed by our group aim to identify triggers, mediators and end-effectors of anesthetic-induced pre- and postconditioning and to characterize their complex intracellular interaction. Given the large incidence of perioperative cardiovascular morbidity and mortality and the incidence of myocardial and cerebral infarction, the results of these projects are of high clinical relevance and might provide a better understanding of the cardioprotective properties of volatile anesthetics. They might help to choose the appropriate and protective anesthesiology regime to alleviate cardiovascular mortality and apoplectic insults in the perioperative period.
Head: Dr. Markus Lange
- Dr. Thorsten Smul
- Dr. Andreas Redel
- Dr. Christopher Lotz (currently at UC Los Angeles)
- Dr. Jan Stumpner
- Dr. Christoph Blomeyer
Visiting Research Fellow
- Dr. Feng Gao
- Tobias Nefzger
- Tobias Tischer-Zeitz
- Johannes Schmidt
- Verena Schnupp
- Anja Frank
- Anna Kellermann
- Nadyia Virstyuk
- Johannes Richl
- Teresa Hilz
- Katerina Pech
- Smul TM, Lange M, Redel A, Stumpner J, Lotz CA, Roewer N, and Kehl F. . pmid:19167913.
- Lange M, Redel A, Lotz C, Smul TM, Blomeyer C, Frank A, Stumpner J, Roewer N, and Kehl F. . pmid:19225392.
- Lange M, Smul TM, Redel A, Lotz C, Jazbutyte V, Schnupp V, Roewer N, and Kehl F. . pmid:18580175.
- Kranke P, Redel A, Schuster F, Muellenbach R, and Eberhart LH. . pmid:18518784.
- Redel A, Lange M, Jazbutyte V, Lotz C, Smul TM, Roewer N, and Kehl F. . pmid:18227289.
- Redel A, Jazbutyte V, Smul TM, Lange M, Eckle T, Eltzschig H, Roewer N, and Kehl F. . pmid:18156310.
- Muellenbach RM, Kredel M, Said HM, Klosterhalfen B, Zollhoefer B, Wunder C, Redel A, Schmidt M, Roewer N, and Brederlau J. . pmid:17563879.
- Lange M, Redel A, Roewer N, and Kehl F. . pmid:17457146.
- Lange M, Smul T, Zimmermann P, Kohlenberger R, Roewer N, and Kehl F. . pmid:17242104.
- Smul TM, Lange M, Redel A, Burkhard N, Roewer N, and Kehl F. . pmid:17006071.
- Lange M, Smul TM, Blomeyer CA, Redel A, Klotz KN, Roewer N, and Kehl F. . pmid:16931983.
- Eckle T, Grenz A, Köhler D, Redel A, Falk M, Rolauffs B, Osswald H, Kehl F, and Eltzschig HK. . pmid:16766632.
- Lange M, Roewer N, and Kehl F. . pmid:16399333.
- Golenhofen N, Redel A, Wawrousek EF, and Drenckhahn D. . pmid:16217658.
- Redel A, Baumgartner W, Golenhofen K, Drenckhahn D, and Golenhofen N. . pmid:12457251.
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