Abstract
We studied in cats the long-term effects upon resting ventilation and the ventilatory responses to CO2 breathing of destruction of neuronal cell bodies within the ventrolateral nucleus of the tractus solitarius (vl-NTS) by kainic acid (KA) injection (KAI). Animals were studied in the awake state and under pentobarbital anesthesia both before and 8 wk after stereotaxic bilateral microinjection of the vl-NTS with mock cerebrospinal fluid (CSF) (controls, n = 2) or with KA in mock CSF (KAI, n = 5). KA reduced the number of cell bodies within the vl-NTS by 75%. Under anesthesia minute ventilation (VI) was reduced by 49% after KAI, due primarily to a 54% reduction in breathing frequency (f). Four of five anesthetized KAI animals exhibited a significantly reduced (P less than 0.01) ventilatory sensitivity to inspired CO2 under anesthesia. In the awake state some KAI animals had significant changes (P less than 0.01) in ventilation; VI reduced (2 of 5), tidal volume reduced (1 of 5), f reduced (3 of 5), and inspiratory and expiratory times increased (2 of 5). Decreases in the awake ventilatory CO2 sensitivity were not significant within individual KAI animals but were significant (P less than 0.05) when considered as a group. Thus following 75% neuronal loss within the vl-NTS, rhythmic ventilation was sustained during both anesthesia and wakefulness, although f was reduced in the former state. The vl-NTS may function to set most but not all of the ventilatory sensitivity to CO2 during anesthesia and to a lesser extent during wakefulness.
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