Ischaemic preconditioning reduces XXXX in transient ischaemia.

@entity23398 @entity95 @entity1514 @entity439 @entity1566 @entity432 @entity451
OBJECTIVE: @entity451 remains a devastating complication after @entity1514 and thoracoabdominal aortic surgery for coarctations, dissections or @entity439 . Since the advent of ischaemic preconditioning of the myocardium, attention has been directed to the nervous system. This study was designed to evaluate the acute protective effect of ischaemic preconditioning on the spinal cord. MEDHODS AND RESULTS: Thirty-six New Zealand white @entity95 were randomly assigned to one of three groups. The preconditioning group had 5 minutes of @entity432 , 25 minutes reperfusion and 20 minutes of ischaemia, whereas the controls had only 20 minutes of ischaemia. The sham group was anaesthetized and subjected to laparotomy without @entity432 . Physiological parameters and somatosensory evoked potentials were monitored during the experiment. Neurological outcome was clinically evaluated up to 48 hour after ischaemia and motor function was scored. Then the animals were sacrificed. Their spinal cord, abdominal aorta and its branches were removed and processed for histopathological examination. Histhopathological changes of the gray matter in the lumbosacral segments were scored from 0 to 6 according to a @entity23398 . The changes in amplitudes of evoked potentials during ischaemia and recovery periods were similar in preconditioning and control groups. The average motor function score was significantly higher in the preconditioning group than the control group at 24 and 48 hours after the ischaemic event (p < 0.05). Histological observations were consistent with the neurological findings. The histopathological scores in the control group and the preconditioning group were 3.2 (1.4-5.2) and 2.4 (0.8-4.4), respectively (p < 0.05). CONCLUSIONS: The results suggest that ischaemic preconditioning reduces the @entity1566 and improves neurological outcome in transient ischaemia in @entity95 . This protective mechanism is rapidly invoked within only 25 minutes interval between the preconditioning stimulus and the ischaemic insult.
