Neuraxial XXXX may trigger transient @entity66 after a noninjurious interval of @entity2759 : a clinical and experimental study.

@entity1 @entity66 @entity63 @entity4218 @entity1746 @entity1510 @entity2334 @entity2759 @entity158 @entity1286 @entity35 @entity451 @entity2332
BACKGROUND: A @entity1 underwent repair of a @entity2334 . Epidural @entity1286 , 4 mg, was given for @entity158 relief. After anesthesia, the @entity1 displayed @entity1746 . This effect was reversed by @entity1510 . The authors sought to confirm these observations using a @entity35 spinal @entity63 model to define the effects of intrathecal @entity1286 administered at various times after reflow on behavior and spinal histopathology. METHODS: @entity2759 was induced for 6 min using an intraaortic balloon. @entity1286 or saline, 30 microg, was injected intrathecally at 0.5, 2, or 24 h after reflow. In a separate group, spinal cord temperature was decreased to 27 degrees C before @entity63 . After @entity63 , recovery of motor function was assessed periodically using the motor deficit index (0 = complete recovery; 6 = complete @entity451 ). RESULTS: After @entity63 , all @entity35 showed near-complete recovery of function by 4-6 h. Intrathecal injection of @entity1286 at 0.5 or 2 h of reflow (but not at 24 h) but not saline caused a development of @entity4218 and lasted for 4.5 h (motor deficit index score = 4-6). This effect was reversed by intrathecal @entity1510 (30 microg). Intrathecal @entity1286 administered after hypothermic @entity63 was without effect. Histopathological analysis in animals that received intrathecal @entity1286 at 0.5 or 2 h after @entity63 (but not at 24 h) revealed dark-staining alpha motoneurons and interneurons. Intrathecal saline or spinal @entity2332 plus @entity1286 was without effect. CONCLUSIONS: These data indicate that during the immediate reflow following a noninjurious interval of spinal @entity63 , intrathecal @entity1286 potentiates @entity66 . Reversal by @entity1510 suggests that this effect results from an opioid receptor-mediated potentiation of a transient block of inhibitory neurons initiated by spinal @entity63 .
