Zhonghua wai ke za zhi [Chinese journal of surgery] · 2000
[Adenosine in treatment of rats with spinal cord injury].
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Zhang Q, Zhao J, Wang Q, Li M, Hou T, Li Z, Zhang L
Аннотация
OBJECTIVE: To observe the changes of endogenous extracellular adenosine after spinal cord injury (SCI) to rats and the effect of exogenous adenosine on extracellular calcium after SCI and post-injury neurological function.
METHODS: A ventral compression injury model of T13 spinal cord was used, and the extracellular fluids were collected consecutively every 20 minutes after injury by using microdialysis. Adenosine in the samples was analyzed using high-pressure liquid chromatography (HPLC) with u.v. detection. The rats received different doses of 2-chloroadenosine (2-CADO), a nonspecific agonist of adenosine receptors, by intrathecal injection 15 minutes before injury. The extracellular fluid was collected every 10 minutes immediately after injury and the calcium was measured using atomic absorption spectrophotometer. Neurological function score, inclined plane angle, and histology were observed 24 hours after injury.
RESULTS: A significant increase of adenosine was found immediately after spinal cord injury. The concentration of adenosine peaked at one hour after injury and dropped down to the basal level. There was a positive relation between the increase of adenosine and the severity of SCI. High dose of 2-CADO can significantly significantly inhibit the decrease of extracellular calcium and improve the neurological function of injured rats.
CONCLUSIONS: Adenosine could involve the pathological process of secondary spinal cord injury and might play a protective role in SCI.
METHODS: A ventral compression injury model of T13 spinal cord was used, and the extracellular fluids were collected consecutively every 20 minutes after injury by using microdialysis. Adenosine in the samples was analyzed using high-pressure liquid chromatography (HPLC) with u.v. detection. The rats received different doses of 2-chloroadenosine (2-CADO), a nonspecific agonist of adenosine receptors, by intrathecal injection 15 minutes before injury. The extracellular fluid was collected every 10 minutes immediately after injury and the calcium was measured using atomic absorption spectrophotometer. Neurological function score, inclined plane angle, and histology were observed 24 hours after injury.
RESULTS: A significant increase of adenosine was found immediately after spinal cord injury. The concentration of adenosine peaked at one hour after injury and dropped down to the basal level. There was a positive relation between the increase of adenosine and the severity of SCI. High dose of 2-CADO can significantly significantly inhibit the decrease of extracellular calcium and improve the neurological function of injured rats.
CONCLUSIONS: Adenosine could involve the pathological process of secondary spinal cord injury and might play a protective role in SCI.