Myocardial Infarct Size-Limiting Effect of Chronic Hypoxia Persists for Five Weeks of Normoxic Recovery

Title:

Myocardial Infarct Size-Limiting Effect of Chronic Hypoxia Persists for Five Weeks of Normoxic Recovery

Creator:

Neckář, J., Ošťádal, B., and Kolář , F

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:8f13f364-22f5-462c-978e-052b97bb9685
uuid:8f13f364-22f5-462c-978e-052b97bb9685

Subject:

chronic hypoxia, Normoxic recovery, Myocardial infarction, Arrhythmias, and Cardioprotection

Type:

article, model:article, and TEXT

Description:

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.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2004 Volume:53 | Number:6

Harvested from:

CDK

Metadata only:

false