Role of ATP-sensitive K(+)-channels in antiarrhythmic and cardioprotective action of adaptation to intermittent hypobaric hypoxia
Language English Country United States Media print
Document type Comparative Study, Evaluation Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
19110582
DOI
10.1007/s10517-008-0106-6
PII: doi
Knihovny.cz E-resources
- MeSH
- Atmospheric Pressure * MeSH
- Cytoprotection drug effects physiology MeSH
- Adaptation, Physiological drug effects physiology MeSH
- Hypoxia pathology prevention & control MeSH
- Imidazoles pharmacology MeSH
- Ischemic Preconditioning, Myocardial methods veterinary MeSH
- KATP Channels agonists physiology MeSH
- Rats MeSH
- Myocardium pathology MeSH
- Altitude MeSH
- Rats, Wistar MeSH
- Arrhythmias, Cardiac prevention & control MeSH
- Thioamides pharmacology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Evaluation Study MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- Imidazoles MeSH
- KATP Channels MeSH
- MCC 134 MeSH Browser
- Thioamides MeSH
Mature Wistar rats were exposed to intermittent hypobaric hypoxia (5000 m, 6 h/day, 30 sessions). This mode of adaptation enhanced heart tolerance to the arrhythmogenic action of 45-min coronary occlusion, but does not affect the infarction size/risk area ratio. In some series, the rats were exposed to more severe intermittent hypobaric hypoxia (7000 m, 8 h/day, 6 weeks) followed by 20-min coronary occlusion and 3-h reperfusion one day after the last hypoxia session. In this case, adaptation reduced the infarction size/risk area ratio and enhanced cardiac tolerance to the arrhythmogenic effect of reperfusion, but had no effect on the incidence of ventricular arrhythmia during ischemia. We found that the cardioprotective and antiarrhythmic effects of adaptation to an altitude of 7000 m and the antiarrhythmic effect of 5000-m adaptation were mediated via activation of K(ATP) channels.
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