The effect of intrathecal administration of NMDA (N-methyl-D-aspartate) receptor antagonists on the isoflurane MAC (minimum alveolar anesthetic concentration), and on the locomotor function, were studied in Wistar rats with catheters placed intrathecally. We determined the isoflurane MAC after the administration of either a competitive NMDA receptor antagonist, AP7 (0.044-132 nmole), or a non-competitive NMDA receptor antagonist, MK801 (0.3-90 nmole), as well as NMDA (0.068-204 nmole), and saline. AP7 (0.44-132 nmole) and MK801 (30-90 nmole) decreased the MAC. Intrathecal administration of NMDA reversed these decreases of MAC, but reversal effect is incomplete with AP7 132 nmole and MK801 90 nmole. In a locomotor dysfunction test, rats showed motor dysfunction with AP7 132 nmole (P < 0.05) and MK801 90 nmole (P < 0.05), but low doses did not exert these effects. Large doses of NMDA antagonist decreased the isoflurane MAC due to motor dysfunction, but low doses reduced the MAC without impairing motor function. We suspect that NMDA receptor antagonists play important roles in determining the isoflurane MAC in the spinal cord.
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