Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Toller, WG; Kersten, JR; Gross, ER; Pagel, PS; Warltier, DC.
Isoflurane preconditions myocardium against infarction via activation of inhibitory guanine nucleotide binding proteins.
Anesthesiology. 2000; 92(5):1400-1407
Doi: 10.1097%2F00000542-200005000-00031
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- Führende Autor*innen der Med Uni Graz
- Toller Wolfgang
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- Abstract:
- BACKGROUND: Isoflurane-induced myocardial protection during ischemia is mediated by adenosine triphosphate-regulated potassium (KATP) channels; however, the intracellular signal transduction cascade responsible for this process has been incompletely evaluated. The authors tested the hypothesis that isoflurane reduces myocardial infarct size through a Gi protein-mediated process. METHODS: Forty-eight hours after pretreatment with vehicle (0.9% saline) or the Gi protein inhibitor pertussis toxin (10 microg/kg intravenously), barbiturate-anesthetized dogs (n = 43) were instrumented for measurement of aortic and left ventricular pressures and maximum rate of increase of left ventricular pressure. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3-h reperfusion. In four separate groups, vehicle- or pertussis toxin-pretreated dogs were studied with or without administration of 1 minimum alveolar concentration isoflurane. In two additional groups, dogs received the direct KATP channel agonist nicorandil (100 microg/kg bolus and 10 microg x kg-1 x min-1 intravenous infusion) in the presence or absence of pertussis toxin pretreatment. Myocardial perfusion and infarct size were measured with radioactive microspheres and triphenyltetrazolium staining, respectively. RESULTS: Isoflurane significantly (P < 0.05) decreased infarct size to 7 +/- 2% of the area at risk compared with control experiments (26 +/- 2%). Pertussis toxin pretreatment alone had no effects on myocardial infarct size (31 +/- 4%) but blocked the beneficial effects of isoflurane (21 +/- 3%). Nicorandil decreased infarct size (11 +/- 2%), but, in contrast to isoflurane, this effect was independent of pertussis toxin pretreatment (11 +/- 1%). CONCLUSION: Isoflurane reduces myocardial infarct size by a Gi protein-mediated mechanism in vivo.
- Find related publications in this database (using NLM MeSH Indexing)
- Anesthetics, Inhalation - therapeutic use
- Animals - therapeutic use
- Dogs - therapeutic use
- GTP-Binding Proteins - drug effects
- Hemodynamic Processes - drug effects
- Ischemic Preconditioning, Myocardial - methods
- Isoflurane - therapeutic use
- Myocardial Infarction - metabolism
- Nicorandil - pharmacology
- Pertussis Toxin - pharmacology
- Potassium Channels - drug effects
- Vasodilator Agents - pharmacology
- Virulence Factors, Bordetella - pharmacology
- Find related publications in this database (Keywords)
- myocardial ischemia
- pertussis toxin