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Selected Publication:
Toller, WG; Gross, ER; Kersten, JR; Pagel, PS; Gross, GJ; Warltier, DC.
Sarcolemmal and mitochondrial adenosine triphosphate- dependent potassium channels: mechanism of desflurane-induced cardioprotection.
Anesthesiology. 2000; 92(6):1731-1739
Doi: 10.1097/00000542-200006000-00033
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- Leading authors Med Uni Graz
- Toller Wolfgang
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- Abstract:
- BACKGROUND: Volatile anesthetic-induced preconditioning is mediated by adenosine triphosphate-dependent potassium (KATP) channels; however, the subcellular location of these channels is unknown. The authors tested the hypothesis that desflurane reduces experimental myocardial infarct size by activation of specific sarcolemmal and mitochondrial KATP channels. METHODS: Barbiturate-anesthetized dogs (n = 88) were acutely instrumented for measurement of aortic and left ventricular pressures. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3-h reperfusion. In four separate groups, dogs received vehicle (0.9% saline) or the nonselective KATP channel antagonist glyburide (0.1 mg/kg intravenously) in the presence or absence of 1 minimum alveolar concentration desflurane. In four additional groups, dogs received 45-min intracoronary infusions of the selective sarcolemmal (HMR 1098; 1 microg. kg-1. min-1) or mitochondrial (5-hydroxydecanoate [5-HD]; 150 microg. kg-1. min-1) KATP channel antagonists in the presence or absence of desflurane. Myocardial perfusion and infarct size were measured with radioactive microspheres and triphenyltetrazolium staining, respectively. RESULTS: Desflurane significantly (P < 0.05) decreased infarct size to 10 +/- 2% (mean +/- SEM) of the area at risk as compared with control experiments (25 +/- 3% of area at risk). This beneficial effect of desflurane was abolished by glyburide (25 +/- 2% of area at risk). Glyburide (24 +/- 2%), HMR 1098 (21 +/- 4%), and 5-HD (24 +/- 2% of area at risk) alone had no effects on myocardial infarct size. HMR 1098 and 5-HD abolished the protective effects of desflurane (19 +/- 3% and 22 +/- 2% of area at risk, respectively). CONCLUSION: Desflurane reduces myocardial infarct size in vivo, and the results further suggest that both sarcolemmal and mitochondrial KATP channels could be involved.
- Find related publications in this database (using NLM MeSH Indexing)
- Adenosine Triphosphate - metabolism
- Anesthetics, Inhalation - antagonists and inhibitors
- Animals - antagonists and inhibitors
- Benzamides - pharmacology
- Decanoic Acids - pharmacology
- Dogs - pharmacology
- Glyburide - pharmacology
- Hemodynamic Processes - drug effects
- Hydroxy Acids - pharmacology
- Hypoglycemic Agents - pharmacology
- Ischemic Preconditioning, Myocardial - pharmacology
- Isoflurane - analogs and derivatives
- Mitochondria - metabolism
- Myocardial Infarction - pathology
- Myocardium - pathology
- Potassium Channel Blockers - pathology
- Potassium Channels - agonists
- Regional Blood Flow - agonists
- Sarcolemma - metabolism
- Find related publications in this database (Keywords)
- myocardial ischemia