| Objective: To investigate the correlation among hyponatremiaand renal sympathetic nerve activity, spinal cord injury degree after acutecervical spinal cord injury in rats. Methods:(1)50adult female Sprague-Dawley (SD) rats with300～350g in weight were randomly divided into fivegroups: injury groups at1day,3days, l week,2weeks and control group.There were10rats in each groups.(2) The cervical spinal cord injury modelswere induced at the level of C7vertebra by dropping a weight of10g from theheight of25mm (Allen’s model). Each rats with0BBB were included. While inthe control group, laminectomy was operated only, leaving spinal cord at thesame level intact.(3) In each groups: the blood samples were collected forassaying blood serum sodium concentration from the caudal vein and theelectrical activity discharge of renal sympathetic nerve were measured.Thesmall intestine propellant rate were observed with ink gastric perfusion methodand the change of spinal cord tissue were observed by HE. The number ofpreserved axons within DRSPs area in adjacent caudal damage segment of thespinal cord (upper thoracic segment) were counted by NF200immunohistochemistry.(4) All the experimental results were documentedby x±s and calculated by SPSS17.0statistical software with single factor analysis of variance, correlation test using Pearson correlation analysis. Results:(1) The serum sodium concentration in injury groups was126.00±4.55mmol/L,124.90±5.09mmol/L,122.50±4.74mmol/L,130.30±6.80mmol/L at1day,3days,1week and2weeks respectively, while it was135.00±5.52mmol/L incontrol group. There was statistical significance between control group andinjury groups at1day,3days and1week respectively(P<0.05), and there was nostatistical significance between control group and injury group at2weeks(P>0.05).(2) The renal sympathetic nerve discharge integral in injury groupswas57.90±5.43μv.s,54.60±4.76μv.s,49.00±6.63μv.s,59.60±3.20μv.s at1day,3days,1week and2weeks respectively, while it was62.00±4.74μv.s in controlgroup. There was statistical significance between control group and injurygroups at1day,3days and1week respectively (P<0.05), and there was nostatistical significance between control group and injury group at2weeks(P>0.05).(3) The small intestine propulsion rate in injury groups was57.60±5.91%,47.00±4.47%,65.10±3.16%,66.40±4.03%at1day,3days,1week and2weeks respectively, while it was67.30±4.57%in control group.There was statistical significance between control group and injury groups at1day and3days respectively(P<0.05), and there was no statistical significancebetween control group and injury groups at1week and2weeks respectively(P>0.05).(4) In the rats suffering from acute cervical spinal cord injury, theserum sodium concentration had significant correlation with the renalsympathetic nerve activity(r=0.664, P<0.001), and the serum sodium concentration had no correlation with the small intestine propulsion rate(r=0.234, P=0.101).(5) There were22rats with hyponatremia, and16rats withnormal serum sodium concentration, so the incidence of hyponatremia was55%in our experiment. The number of preserved axons within DRSPs was140.90±5.78/10000μm2,46.94±11.69/10000μm2,30.82±11.82/10000μm2in control group, normonatremic SCI group, and hyponatremic SCI grouprespectively. The number of preserved axons within DRSPs in normonatremicSCI group was more than hyponatremic SCI group, while it was less thancontrol group. There was statistical significance among control group,hyponatremic SCI group and normonatremic SCI group (P<0.05). Conclusion:(1) The hyponatremia after acute cervical spinal cord injury is correlated withrenal sympathetic nerve excitability, maybe it is due to the restraint of renalsympathetic nerve.(2) Whether the hyponatremia will occur or not after acutecervical spinal cord injury depends on the number of preserved axons withinDRSPs area. |
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