The primary mechanism of action of the spinal anesthetic ketamine is noncompetitive blocking of the NMDA ionophore. Widespread use of bupivacaine for pain management

Spinal anesthesia or regional anesthesia is a potent anesthetic procedure. Additional modalities have been sought to increase the duration of block in spinal anesthesia. Ketamine is an N-methyl-D-aspartate (NMDA) receptor blocker that has an anesthetic effect when injected intrathecally and has a synergic effect with bupivacaine. Ketamine also has potent analgesic properties. The present study investigated the effect of intrathecally administered ketamine on spinal anesthesia with levobupivacaine or ropivacaine. Sprague-Dawley rats at post-natal day 21 were exposed to spinal anesthesia with 0.5% levobupivacaine or 0.5% ropivacaine. Separate groups of rats were treated with intrathecal ketamine at a 5 or 10 mg/kg bodyweight dose along with ropivacaine or levobupivacaine. The thermal and mechanical withdrawal latencies of the animals were determined using hot plate and von Frey filaments, respectively. A rotarod apparatus was employed to assess the capacity of the rats to rotate the spindle at 24 h following anesthesia. The gait of the rat pups was also assessed. Intrathecal administration of ketamine resulted in dense blocks and extended the duration of spinal blocks as evidenced by thermal latencies and responses to von Frey filaments. The latency to fall was shorter in rats exposed to ketamine along with ropivacaine or levobupivacaine spinal anesthesia. The gait parameters were also more disturbed upon ketamine administration. In conclusion, ketamine administration with ropivacaine or levobupivacaine increased the intensity and duration of spinal blockade, thereby increasing the anesthetic effects.