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1Internal Medicine and 2Psychology, University of Iowa, Iowa City 55242; and 3Veterans Affairs Medical Center, Iowa City, Iowa 52242
Submitted 10 November 2003 ; accepted in final form 26 January 2004
The inflammatory milieu of acute myocardial infarction (MI) is theoretically conducive to enhanced cytokine synthesis within the brain. We tested the hypothesis that synthesis of tumor necrosis factor-
(TNF-), an indicator of proinflammatory cytokine activity, increases in brain after MI. MI was induced in rats by ligating the left anterior descending coronary artery and confirmed by echocardiography. Plasma and tissue levels of TNF- were measured using ELISA; TNF- mRNA was measured with real-time PCR. Heart, brain, and plasma samples were obtained 0.5, 1, 4, or 24 h or 4 wk after MI. TNF- synthesis increased in the brain, heart, and plasma within minutes to hours after MI and was sustained over the interval tested. Among the brain tissues examined, TNF- increased selectively in hypothalamus. Chronic treatment with pentoxifylline prevented the increases in TNF- in brain, heart, and plasma measured 4 wk after MI. MI-induced cytokine synthesis in the hypothalamus and its prevention by pentoxifylline have important implications in the context of the development of heart failure after MI.
tumor necrosis factor-; sympathetic nerve activity; hypothalamic-pituitary-adrenal axis; heart failure
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