2007Unpublished venueRequires access

The Reperfusion Injury Model Improvement and the Tolerance Time Investigation of Rabbit Spinal Cord Ischemia under Normothermia

LI Jian-shu

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Abstract

Objective This study is designed to improve the rabbit model of ischemic- reperfusion injury and determine the safe clamping duration relevant to the spinal cord tolerance to ischemia at normothermia. Methods 50 New Zealand white rabbits were assigned randomly to 5 groups (Group C20, C25, C30, C40 and C60, 10 rabbits in each group) according to different clamping durations, ranging from 20 min to 60 min. The rabbits were endotracheally intubated for ventilation, and their left ear arteries were catheterized for monitoring the mean artery pressure. The spinal cord ischemia was induced by infrarenal aorta occlusion. A catheter was inserted into the aorta distal clamped site for monitoring the distal artery pressure. The neurological functional status of animal was assessed with the Tarlov scale system (0 or 1 meaning the rabbit paraplegia), at the moment of revival, 6 h, 24 h, and 48 h after the reperfusion. After last scoring, the lumbar segments of spinal cord (L4-L6) were removed for pathological examination, and the normal motor neurons of anterior horn were counted. Results Forty-eight hours after the infusion, the severe neurological impairments were not detected in the rabbits whose aorta were only clamped for 20 min (Group C20). However, the rabbits in Group C60 became totally paraplegic, and the rabbits in Group C25, C30 or C40 developed the paraplegia at 30%, 80% or 90% respectively. The median number of normal motor neuron was 12.5, 10 or 2 respectively in Group C20, C25 or C30, and 0 median number resulted in Group C40 and C60. Conclusion The rabbit model of ischemic-reperfusion injury is successfully improved, of which the safe clamping duration without spinal cord injury is not more than 20 min at normothermia.

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Objective This study is designed to improve the rabbit model of ischemic- reperfusion injury and determine the safe clamping duration relevant to the spinal cord tolerance to ischemia at normothermia. Methods 50 New Zealand white rabbits were assigned randomly to 5 groups (Group C20, C25, C30, C40 and C60, 10 rabbits in each group) according to different clamping durations, ranging from 20 min to 60 min. The rabbits were endotracheally intubated for ventilation, and their left ear arteries were catheterized for monitoring the mean artery pressure. The spinal cord ischemia was induced by infrarenal aorta occlusion. A catheter was inserted into the aorta distal clamped site for monitoring the distal artery pressure. The neurological functional status of animal was assessed with the Tarlov scale system (0 or 1 meaning the rabbit paraplegia), at the moment of revival, 6 h, 24 h, and 48 h after the reperfusion. After last scoring, the lumbar segments of spinal cord (L4-L6) were removed for pathological examination, and the normal motor neurons of anterior horn were counted. Results Forty-eight hours after the infusion, the severe neurological impairments were not detected in the rabbits whose aorta were only clamped for 20 min (Group C20). However, the rabbits in Group C60 became totally paraplegic, and the rabbits in Group C25, C30 or C40 developed the paraplegia at 30%, 80% or 90% respectively. The median number of normal motor neuron was 12.5, 10 or 2 respectively in Group C20, C25 or C30, and 0 median number resulted in Group C40 and C60. Conclusion The rabbit model of ischemic-reperfusion injury is successfully improved, of which the safe clamping duration without spinal cord injury is not more than 20 min at normothermia.

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Available abstract

Objective This study is designed to improve the rabbit model of ischemic- reperfusion injury and determine the safe clamping duration relevant to the spinal cord tolerance to ischemia at normothermia. Methods 50 New Zealand white rabbits were assigned randomly to 5 groups (Group C20, C25, C30, C40 and C60, 10 rabbits in each group) according to different clamping durations, ranging from 20 min to 60 min. The rabbits were endotracheally intubated for ventilation, and their left ear arteries were catheterized for monitoring the mean artery pressure. The spinal cord ischemia was induced by infrarenal aorta occlusion. A catheter was inserted into the aorta distal clamped site for monitoring the distal artery pressure. The neurological functional status of animal was assessed with the Tarlov scale system (0 or 1 meaning the rabbit paraplegia), at the moment of revival, 6 h, 24 h, and 48 h after the reperfusion. After last scoring, the lumbar segments of spinal cord (L4-L6) were removed for pathological examination, and the normal motor neurons of anterior horn were counted. Results Forty-eight hours after the infusion, the severe neurological impairments were not detected in the rabbits whose aorta were only clamped for 20 min (Group C20). However, the rabbits in Group C60 became totally paraplegic, and the rabbits in Group C25, C30 or C40 developed the paraplegia at 30%, 80% or 90% respectively. The median number of normal motor neuron was 12.5, 10 or 2 respectively in Group C20, C25 or C30, and 0 median number resulted in Group C40 and C60. Conclusion The rabbit model of ischemic-reperfusion injury is successfully improved, of which the safe clamping duration without spinal cord injury is not more than 20 min at normothermia.

Key concepts: Medicine, Paraplegia, Anesthesia, Spinal cord, Ischemia, Aorta, Reperfusion injury, Abdominal aorta

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