Neuroprotective Effects of Ketamine in a Rodent Model of Peptide Induced SpinalCord Injury: Anatomical and Physiological Correlates

摘要

Dynorphin A (1-17) D Y N is an endogenous peptide which produces spinal cordischemia, nociceptive loss and hindlimb paralysis when injected into the lumbar cistern of unanesthetized or halothane anesthetized rats. We initially noted that ketamine (K) when used as the anesthetic agent during routine recording of somatosensory evoked potentials (SEP) preserved the SEP cortical response and affected the neurologic outcome in the previously reported paralytic dose (20 nM, DYN) was used. Subsequently we reported that K and other N M D A receptor antagonists in the neurologic recovery following D Y N injection. The current study was divided into two experiments. The first, a neuroanatomical study divided into Groups I-IV, were performed in adult Sprague Dawley rats anesthetized with halothane. The i.t. dose of D Y N was 20 mm for all animals. A lumbar subarachnoid (i.t.) injection of saline (I), D Y N alone (20 nM, II) D Y N plus K (4nM, III) and D Y N plus K (2nM, IV). The animals were neurologically evaluated for 72 hours, anesthetized and perfused per cardia with formalin and the lumbosacral cord removed. (jes)