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Background: Anxiodepressive symptoms were associated with a significantly higher risk of fatal
cardiovascular events. This appear to be attributable largely to an increase in sudden
cardiac death, predicted by high sympathetic activity and decrease in heart rate variability.
However, the central mechanism involved in this pathological alteration remained unknown.
The dorsal medial nucleus of the hypothalamus (DMH) is part of acute arousal responses
in stress (defense) situation, and its stimulation induces an increase in sympathetic
activity. Our aim was to study the possible role of the DMH in the sympathetic alterations
in chronic stress.
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