Myocardial Infarct
Size-Limiting Effect of Chronic Hypoxia
Persists for Five Weeks of Normoxic Recovery
J. NECKÁŘ, B. OŠŤÁDAL, F. KOLÁŘ
Institute of Physiology, Academy of Sciences of the Czech
Republic and Centre for Experimental Cardiovascular Research,
Prague
Received September 27, 2003
Accepted September 30, 2004
Summary
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.
Key words
Chronic hypoxia • Normoxic recovery • Myocardial infarction •
Arrhythmias • Cardioprotection
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