Inhibitory effect of 6-hydroxy dopamine and MK-801 on spinal cord edema / 中国组织工程研究

ABSTRACT

BACKGROUND: After acute spinal cord injury (SCI), edema of spinal cord is an important factor for inducing and deteriorating pathological changes of spinal cord tissue. After injury, noradrenaline (NE) instantly causes microvascular contraction, endothelial injury, increase of arterial permeability and participation in edema. Recently, many researches suggest that excitatory amino acids (EAA) are related to cellular edema.OBJECTIVE: To study the effect and mechanism of selective phenol aminergic neuron, 6-hydroxy dopamine (6-OHNA)and aspartic acid (ASP) on edema after acute SCI.DESIGN: Randomized controlled study.SETTING: Department of Spine Surgery, the Third Hospital of Hebei Medical University.MATERIALS The experiment was carried out at the Experimental Animal Center of the Third Hospital of Hebei Medical University from March to September 2003. A total of 160 Wistar rats weighing 300-350 g of both genders were randomly divided into three groups 6-OHNA group (n =60), MK-801 group (n =50) and control group (n =50).METHODS: Acute SCI was induced at the level of T13 vertebral body with the static lcad technique. Rats in 6-OHNA group were injected with 6-OHNA into subarachnoid space; rats in MK-801 group were injected with MK-801 into caudal vein; rats in control group did not receive any treatment. The extent of edema was compared in the three groups by means of neurological scoring, water content measurement, light microscopy and electron microscopy.MAIN OUTCOME MEASURES: Neurological scores and water content.RESULTS: All 160 rats were involved in the final analysis. ① After SCl, content of NE in 6-OHNA group was decreased from (217.45±4.26) ng/g to (29.37±2.61) ng/g, and the difference was significant (P＜ 0.01). Edema in spinal cord tissue was effectively inhibited for 24 hours. At 12 hours after SCl, function recovered remarkably and vascular-derived edema was the mildest. ② In MK-801 group, there was no significant suppression of the edema until 24 hours after injury. Early recovery of neurological function was not significantly different from that in control group (P ＞ 0.05), but functional recovery was obvious until 24 hours after injury (P＜0.05). The degree of cytotoxic edema was the lightest.CONCLUSTON NE can inhibit vascular-derived edema at early phase of SCI, and EAA can inhibit cytotoxic edemas,which develops at a relatively later stage.