1Department of Orthopaedics, the First Affiliated Hospital of Liaoning Medical University, Jinzhou   121000, Liaoning Province, China

2Emergency Department, the First Affiliated Hospital of Liaoning Medical University, Jinzhou   121000, Liaoning Province, China

3Department of Endocrinology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou   121000, Liaoning Province, China

Xifan Mei☆, Doctor, Associate professor, Department of Orthopaedics, the First Affiliated Hospital of Liaoning Medical University, Jinzhou  121000, Liaoning Province, China Supported by: Tackle Key Problem Plan of Science and Technology in Liaoning Province, No.2004225003-8* Mei XF, Wang YS, Liu C. Protective effects of prostaglandin E1 perfusion against spinal cord ischemia-reperfusion injury in a rabbit model. Neural Regen Res 2008;3(6):659-62

Abstract

BACKGROUND: Prostaglandin E1 (PGE1) is known to be protective in ischemia-reperfusion of heart, lung, renal, and liver tissue. It still remains to be determined whether PGE1 exhibits similar protection against spinal cord ischemia-reperfusion injury in a rabbit model.

OBJECTIVE: To observe the large, ventral horn, motor neurons of the spinal cord, as well as limb function, and to investigate whether perfusion of PGE1 exhibits protective effects against spinal cord ischemia-reperfusion injury in a rabbit model.

DESIGN, TIME AND SETTING: Controlled observation. The experiment was performed at the Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University between June and October 2007.

MATERIALS: Twenty male, New Zealand white rabbits, weighing 2.0 kg and of mixed gender, were used in the present study. The following chemicals and compounds were used: prostaglandin E1 injectable powder, as well as malondialdehyde and ATPase kits. Animal intervention was in accordance with animal ethical standards.

METHODS: We separated rabbits into control and experimental groups randomly, with 10 rabbits in each group. Rabbits were used as spinal cord ischemia models by segmentally cross-clamping the infrarenal aorta. The control group was subsequently perfused for five minutes with blood and saline solution, and the experimental group was perfused for 5 minutes with blood and saline solution containing PGE1   (100 ng/kg/min).

MAIN OUTCOME MEASURES: The neurological function of the hind limbs was assessed 12, 24, and 48 hours after model establishment. All animals were sacrificed and spinal cords were harvested for histological analyses. The large motor neurons in the ventral horn of L_1-7 were observed by inverted microscope.

RESULTS: All 20 rabbits were included in the final analysis, without any loss. In the ventral horn of the L_5-7 segments, there were more large motor neurons that appeared viable in the experimental group than the control group (P < 0.05). The scores of hind limb functions were greater in the experimental group after 12, 24, and 48 hours (P < 0.01).

CONCLUSION: Perfusion of PGE1 reduced the amount of neuronal damage in the spinal cord ischemia-reperfusion injury rabbit model. These results correlated with increased numbers large motor neurons in the ventral horn of the spinal cord, as well as improved hind limb function.

Key Words: prostaglandin E1; spinal cord; ischemia-reperfusion; neuron

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