Hypothalamus mediates the cardiovascular changes induced by insular epilepsy

To investigate the role of the hypothalamus in cardiovascular changes induced by insular epilepsy. We observed changes in heart rate (HR), blood pressure (BP), and concentration of plasma noradrenaline (NA) in a rat model of insular epilepsy by blocking hypothalamus activity. Insular epilepsy was induced by injecting kainic acid (KA) into the insular cortex. The activities in the bilateral hypothalamus were blocked by electrical lesion. The HR, BP, and concentration of plasma NA were examined in the control group (A), insular epilepsy group (B), hypothalamus lesion alone group (C) and hypothalamus lesion plus insular epilepsy group (D). Insular epilepsy significantly increased the HR, BP, and concentration of plasma NA compared with those in the control group and hypothalamus lesion alone group. Whereas an increase in HR, BP, and the concentration of NA by insular epilepsy were prevented by hypothalamus lesion. The insular cortex mediates the cardiovascular changes during epilepsy mainly through the hypothalamus. These results provide potential therapeutic strategy for insular epilepsy patients with cardiovascular diseases.