Related Experiment Video
Updated: Oct 1, 2026

Experimental Strategies to Bridge Large Tissue Gaps in the Injured Spinal Cord after Acute and Chronic Lesion
Published on: April 5, 2016
Functional recovery of the spinal cord following ischemia and reperfusion injury
Bo Liu1, Zhengyi Sun, Weihong Liao
1Institute of Orthopedics, Second Affiliated Hospital, Lanzhou Medical College, Lanzhou 730030, China. liuo1970@sina.com
Objective:
To study the changes of excitatory amino acids (EAAs) and intracellular calcium ([Ca2+]i), and the protective effect of EAAs receptor antagonists in the tissues of rabbit lumbar spinal cord after 40-minues ischemia and 4-hours reperfusion.
Methods:
Thirty healthy rabbits were divided into six groups: sham-operation, 40-minues ischemia, 4-hour reperfusion, ketamine and MgSO4 treatment, ketamine treatment, and saline treatment groups. The contents of EAAs (glutamate and aspartate) and [Ca2+]i were measured.
Results:
The contents of glutamate and aspartate were decreased to 15.18 micromol/g+/-2.33 micromol/g and 9.99 micromol/g+/-0.69 micromol/g, respectively; 13.75 micromol/g+/-2.58 micromol/g and 6.49 micromol/g+/-1.39 micromol/g after reperfusion. In the ischemia group, the [Ca2+]i was elevated to 221.2 microg/g+/-4.27 microg/g, and elevated further to 298.3 microg/g+/-9.26 microg/g after reperfusion, being significantly higher than that of ischemia and control groups. Ketamine could obviously increase the level of glutamate and aspartate and decrease the level of [Ca2+]i during the ischemia and reperfusion injury.
Conclusions:
The excitotoxicity of EAAs and the overload of calcium induced by EAAs play a harmful role in ischemia and reperfusion injury. Ketamine has an effective inhibitory effect.
Related Concept Videos
Secondary Spinal Cord Injury llI: Pathophysiology
Neurogenesis and Regeneration of Nervous Tissue
Spinal Cord Injury ll: Pathophysiology

