Abstract
It has been reported that tumor necrosis factor (TNF‐α) can precondition the heart against acute ischemia/reperfusion injury. This study examined if TNF‐α also plays a role in a long‐lasting cardioprotection induced by chronic hypoxia. Adult male Wistar rats were exposed for 30 days to chronic continuous hypoxia (CCH; inspired O2 fraction 0.1); half of the animals were treated with a TNF‐α inhibitor infliximab (5 mg/kg i.p. once a week). Controls were kept at room air and treated in a corresponding manner. CCH increased the concentration of TNF‐α in particulate fraction of the left ventricle while the concentration of interleukin 10 (IL‐10) and the ratio of IL‐10 to TNF‐α decreased in both cytosolic and particulate fractions. Myocardial infarct size induced by 20‐min coronary artery occlusion and 3‐h reperfusion was reduced in CCH rats by 33% as compared with normoxic controls. This protective effect was attenuated in animals treated with infliximab, which had no effect in normoxic controls. The results suggest that adaptation to CCH results in the myocardial inflammatory response and TNF‐α is involved in the cardioprotective mechanism.Supported by grants GAAV IAAX01110901, GACR 303/12/1162.
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