Myocardial infarct size-limiting effect of chronic hypoxia persists for five weeks of normoxic recovery
Language English Country Czech Republic Media print
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
15588130
Knihovny.cz E-resources
- MeSH
- Chronic Disease MeSH
- Ventricular Fibrillation diagnosis etiology physiopathology MeSH
- Adaptation, Physiological MeSH
- Risk Assessment methods MeSH
- Hypoxia complications pathology physiopathology MeSH
- Incidence MeSH
- Myocardial Infarction etiology pathology physiopathology MeSH
- Rats MeSH
- Recovery of Function physiology MeSH
- Rats, Wistar MeSH
- Risk Factors MeSH
- Severity of Illness Index MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
We examined cardioprotective effect of chronic hypoxia and the time course of its recovery under normoxic conditions. Adult male Wistar rats were exposed to intermittent hypobaric hypoxia (7000 m, 8 h/day, 35 exposures) and susceptibility of their hearts to ischemia-induced ventricular arrhythmias and myocardial infarction was evaluated in anesthetized open-chest animals subjected to 30-min coronary artery occlusion and 4-h reperfusion on the day after the last hypoxic exposure and at 7, 35 and 90 days of normoxic recovery. The infarct size was reduced from 69.2+/-1.7 % of the area at risk in normoxic controls to 48.0+/-2.2 % in the chronically hypoxic group and to 61.6+/-2.3 % in the group recovered for 7 days. This residual protection persisted for at least 35 days of normoxic recovery but it was absent after 90 days. In contrast to the infarct size-limitation, the antiarrhythmic protection disappeared already during the first week; the incidence of ventricular fibrillation was even significantly increased 7 and 90 days after the last hypoxic exposure. In conclusion, the duration of cardioprotection induced by chronic hypoxia differs markedly, depending on the end point of ischemia/reperfusion injury examined. Whereas the increased tolerance to lethal myocardial injury persists for at least 5 weeks after the termination of hypoxia, the antiarrhythmic protection rapidly vanishes, being replaced with transient proarrhythmic effect.
Selection of optimal reference genes for gene expression studies in chronically hypoxic rat heart
