Neuroprotective effect of 1-aminocyclopropanecarboxylic acid in a rabbit spinal ischemia model

H Unno, T Jikuya, T Yamamoto, Y Sakakibara
Thoracic and Cardiovascular Surgeon 2005, 53 (3): 133-7

BACKGROUND: Postoperative paraplegia remains a serious complication after repair of a thoracoabdominal aortic aneurysm. The release of the excitatory neurotransmitter glutamate might be responsible for ischemic neuronal damage. We investigated the effect of 1-Aminocyclopropanecarboxylic acid (ACPC) on the prevention of paraplegia in a rabbit model of spinal cord ischemia.

METHODS: The infrarenal abdominal aorta was clamped in eighteen rabbits. Saline (group A), 20 mg/kg of ACPC (group B), or 10 mg/kg of ACPC (group C), was injected into the clamped aorta. The animals were neurologically evaluated by Tarlov's score. The spinal cord was obtained for histopathologic examination, including hematoxylin and eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining method.

RESULTS: Postoperative complete paraplegia with marked neuronal necrosis appeared in group A animals. Four of the six group C animals showed intact neurological function. Scattered TUNEL positive neurons were seen within areas containing necrotic cells in sections from paraplegic animals in group A.

CONCLUSIONS: ACPC can prevent spinal cord injury in a rabbit model of spinal cord ischemia.

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