ObjectiveTo review the advances of the role of mitochondrial dysfunction in the spinal cord injury (SCI) and its relevant treatments. MethodsFocusing on various mechanisms of mitochondrial dysfunction, recent relevant literature at home and abroad was identified to summarize the therapeutic strategies for SCI. ResultsMitochondrial dysfunction is mainly manifested in abnormalities in mitochondrial energy metabolism, mitochondrial oxidative stress, mitochondrial-mediated apoptosis, mitophagy, mitochondrial permeability transition, and mitochondrial biogenesis, playing a vital role in the development of SCI. Drug that enhanced mitochondrial function have been proved beneficial for the treatment of SCI. ConclusionMitochondrial dysfunction can serve as a potential therapeutic target for SCI, providing ideas and basis for the development of SCI therapeutic candidates in the future.
ObjectiveTo study the feasibility and advantages of preparing an animal model of defecation reconstruction after spinal cord injury in rats by mechanical polishing method. MethodsForty adult female Sprague Dawley rats (weighing, 250-300 g) were randomly divided into 2 groups (n=20). The lamina was opened by mechanical polishing method to expose the cauda equina in experimental group, then bilateral L5 and S1 nerve roots end-to-end anastomosis was done under 10 times microscope, and finally cauda equina between the L5 and L6 (except S1) was cut. The lamina was opened by traditional bites method in control group, and the other treatment methods were in agreement with the experimental group. The operative time, intra-operative blood loss, and situation of rats at postoperative 3 days were recorded. ResultsThe operative time of experimental group[(93.05±7.60) minutes] was significantly shorter than that in control group[(131.30±11.68) minutes] (t=12.279, P=0.000); intra-operative blood loss in experimental group[(4.33±0.46) mL] was significantly lower than that in control group[(7.36±0.58) mL] (t=18.293, P=0.000). At 3 days after operation, 18 rats (90%) survived in experimental group, and 12 rats (60%) survived in control group; difference was significant in the survival rate between 2 groups (χ2=4.800, P=0.028). ConclusionTo establish an animal model of defecation reconstruction after spinal cord injury in rats by mechanical polishing method is feasible, and it has shorter operative time, less blood loss, and lower postoperative mortality than the traditional bites method. But there is a certain learning curve and requirement to master microsurgical techniques.
Objective Bone marrow mesenchymal stem cells (BMSCs) play an important role in repairing nerve injury, meanwhile external temperature has significant effect on BMSCs transplantation, prol iferation, and differentiation. To investigate the effect of BMSCs transplantation and mild hypothermia on repair of rat spinal cord injury (SCI). Methods Forty-five female adult SD rats (weighing 200-250 g) were made the models of hemitransection SCI and divided randomly into 3 groups according to different treatments: group A (SCI group), group B (BMSCs transplantation group), and group C [BMSCs transplantation combined with mild hypothermia (33-35 ) group]. At 1, 2, 4, 6, and 8 weeks after injury, the fuction of hind l imb was evaluated with Basso Beattie and Bresnahan (BBB) score and incl ined plane test. At 4 weeks after injury, histopathology and BrdU immunohistochemistry staining were performed. At 8 weeks after injury, horseradishperoxidase (HRP) retrograde nerve trace and transmission electron microscope (TEM) testing were performed to observe the regeneration of axon. Results After 4 weeks, the function of hind l imb obviously recovered in groups B and C, there were significant differences in BBB score between groups B, C and group A (P lt; 0.05), between group B and group C (P lt; 0.05). There was no significant difference (P gt; 0.05) in tilt angle among 3 groups after 1 and 2 weeks, and there were significant differences (P lt; 0.05) among 3 groups after 4 weeks. HE staining showed that significant cavity could be seen in group A, l ittle in group B, and no cavity in group C. BrdU immunohistochemistry staining showed that the number of positive cells was 0, 90.54 ± 6.23, and 121.22 ± 7.54 in groups A, B, and C, respectively; showing significant differences (P lt; 0.01) among 3 groups. HRP retrograde neural tracing observation showed that the number of HRP positive nerve fibers was 10.35 ± 1.72, 43.25 ± 2.65, and 84.37 ± 4.59 in groups A, B, and C, respectively, showing significant differences (P lt; 0.01) among 3 groups. TEM observation showed that a great amount of unmyel inated nerve fibers and myel inated nerve fibers were found in central transverse plane in group C. Conclusion The BMSCs transplantation play an impontant role in promotion of recovering the function of hind l imb after SCI, and mild hypothermia has synergism effects.
Objective To establish the artificial bladder reflex arc by the normal body reflex pathway above the horizon of spinal cord injury to reinnervate the flaccid bladder and restore bladder micturition function. Methods An intradural microanastomosis was performed on the L6 ventral root tothe S2 ventral root. After axonal regeneration,the “patellar ligament-spinal cord center-bladder” reflex pathway was reestablished. A longterm function of the reflex arc was observed in the nerve electrophysiological experiment, detrusor electromyography experiment, and urodynamic testing 8 months after anastomosis. Results Trains of the stimuli(200 μV,5 ms) in the left L6 dorsal root and the nerve at the anastomosizedsite resulted in motor evoked potential from the disal to the anastomosized site before and after the spinal cord was destroyed horizontally between S1 and S4 segment levels in 2 Beegle dogs.The figure and amplitude of the evoked potential were similar to those of the control and general stability which showed anoninterventional wave. The urodynamic test revealed a rapid increase of the bladder pressure and a minor increase in the abdominal pressure. This showed that the bladder detrusor mainly resulted in the pressure increase.The bladder pressure increased to 60% of the normal on average compared with the controls when resulted in the left L6 dorsal root and the nerve anastomosized site were stinulated. Conclusion The long-term observation by the nerveelectrophysiological experiment, detrusor electromyography experiment, and urodynamic test indicate that the new artificial reflex arc can be established successfully. The somatic motor axons can regenerate into the parasympathetic endoneurial tubes of the autonomic nerve.
OBJECTIVE: To investigate the etiology, pathological mechanism and treatment of cervical fracture-dislocation without spinal cord injury. METHODS: Nine patients with cervical fracture-dislocation without spinal cord injury were male and aged 22 to 63 years. Based on the clinical symptoms and roentgenographic changes, the injury mechanism was analyzed; and the pathological characteristics and treatment principle were put forward. RESULTS: Anterior reduction was employed in all 9 cases. Eight cases were reduced completely while 1 case was reduced partially. After following up 1 to 3 years, 7 cases recovered completely and the other 2 cases relieved their symptoms obviously. No nervous symptoms aggravated during the following-up period. CONCLUSION: Fracture-dislocation of the cervical spine without spinal cord injury has special pathological mechanism. The surgical intervention is needed for solid fixation and complete decompression without any delayed neurosymptoms.
Objective To investigate the feasibil ity of establ ishment of physiological micturition reflex arc by simultaneously reconstructing the sensory and the motorial nerve of atonic bladder after spinal cord injury. Methods Eight 1-year-old Beegle male canine were selected, weighing 7-12 kg. The left side was the experimental side, while the right side wasthe control side. Epidural microanastomosis of vertebral canal of the left L7 ventral root to S2 ventral root and L7 dorsal root to S2 dorsal root was performed to reconstruct the sensory and the motorial function of atomic bladder. The right side was used as a control without treatment. The new motor-to-motor, and sensory-to-sensory physiological bladder reflex pathway were establ ished after 12 months of axonal regeneration. Then S1-4 segmental spinal cord was destroyed for preparation of complete paraplegia. The electrophysiological examination and the bladder pressure were detected before and after paraplegia. The canine micturition was observed for 3 months after paraplegia. Nurohistological observation was performed after canine sacrifice. Results Of 8 canine, 7 canine survived. After paraplegia, canines displayed urinary incontinence and frequent micturition at first, nocturnal continence was achieved gradually without frequent micturition after 1 month. Urinary infection at different degrees occurred in 3 canines and was controlled after Norfloxacin was administered orally. The bladder pressure increased to (1.00 ± 0.13) kPa, (0.90 ± 0.12) kPa after trains of stimulation (300 mV, 0.3 ms, 20 Hz, 5 seconds) of S2 dorsal root at the experimental side before and after paraplegia respectively, showing no significant difference (P gt; 0.05). It increased to (1.90 ± 0.10) kPa after the same train of stimulation of S2 dorsal root at control side. There was significant difference between the experimental side and the control side (P lt; 0.01). Single stimulation (300 mV, 0.3 ms) of the S2 dorsal root at the experimental side resulted in evoked potentials recorded from the left S2 ventral root before and after paraplegia. Before and after paraplegia, the ampl itudes of the evoked potentials were (0.68 ± 0.11) mV and (0.60 ± 0.08) mV respectively, showing no significant difference (P gt; 0.05). It was (1.21 ± 0.13) mV while stimulating at the control side. There was significant difference between the experimental side and the control side (P lt; 0.01). Neurofibra of L7 dorsal and ventral root grew into S2 dorsal and ventral root on tissue sl ice under l ight microscope. Conclusion Reconstruction of the bladder physiological micturition reflex arc is feasible by anastomosis of sacral dorsal and ventral root below injured spinal plane with the suprasacral survival dorsal and ventral root above the plane respectively for restoration of atonic bladder after spinal cord injury.
ObjectiveTo explore the influence of evidence-based nursing care of catheterization on the incidence of urinary tract injury and urinary tract infection in patients with spinal cord injury and long-term indwelling catheters.MethodsFrom July 1st, 2017 to November 30th, 2018, 100 patients with spinal cord injury indwelling catheters in Department of Spinal Surgery were prospectively selected as the research objects. According to the admission time, patients admitted between July 2017 and February 2018 were assigned into the control group (n=50), and patients admitted between March 2018 and November 2018 were assigned into the observation group (n=50). Traditional catheter placement was used in the control group, while evidence-based catheter placement was used in the observation group. The incidences of catheter-related urethral injury and urinary tract infection after the catheterization were compared between the two groups.ResultsThere was no statistically significant difference in gender, age, diagnosis, or length of hospital stay between the two groups (P>0.05). Catheter placement was performed 57 times in the control group and 59 times in the observation group during hospitalization. After catheterization, the incidences of urethral hemorrhage and gross hematuria in the control group [22.80% (13/57) and 15.78% (9/57), respectively] were higher than those in the observation group [both were 1.69% (1/59)], with statistical differences between the two groups (P<0.05). The incidence of urinary tract infection in the control group differed from that in the observation group [42.0% (21/50) vs. 18.0% (9/50), P=0.009].ConclusionThe evidence-based urinary catheterization method for patients with spinal cord injury and long-term indwelling catheter can effectively prevent catheter-related urinary tract injury, reduce the incidence of catheter-related urinary tract infection during hospitalization, and improve the quality of clinical care.
ObjectiveTo explore the biological functions of Kip1 ubiquitylation-promoting complex 2 (KPC2) in the repair process of spinal cord injury (SCI) by studying the expression and cellular localization of KPC2 in rat SCI models. MethodsFifty-six adult Sprague-Dawley rats were randomly divided into 2 groups: in the control group (n=7), simple T9 laminectomy was performed;in the experimental group (n=49), the SCI model was established at T9, 7 rats were used to detect follow indexs at 6 hours, 12 hours, 1 day, 3 days, 5 days, 7 days, and 14 days after SCI. Western blot analysis was used to detect the protein expressions of P27kip1, KPC2, CyclinA and proliferating cell nuclear antigen (PCNA) after SCI. Immunohistochemistry was used to observed the cellular localization of KPC2 after SCI, double-labeling immunofluorescence staining to observe the co-localization of KPC2 with neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP) and PCNA. in vitro astrocytes proliferation model was used to further validate these results, Western blot to detect KPC2, P27kip1, and PCNA expressions. The interaction of P27kip1, KPC1, and KPC2 in cell proliferation was analyzed by co-immunoprecipitation. ResultsThe Western blot analysis showed a significant down-regulation of P27kip1 and a concomitant up-regulation of KPC2, CyclinA, and PCNA after SCI. Immunohistochemistry staining revealed a wide distribution of KPC2 positive signals in the gray matter and white matter of the spinal cord. The number of KPC2 positive cells in the experimental group was significantly higher than that in the control group (t=10.982, P=0.000). Double-labeling immunofluorescence staining revealed the number of KPC2/NeuN co-expression cells in the gray matter of spinal cord was (0.43±0.53)/visual field in the control group and (0.57±0.53)/visual field in the experimental group, showing no significant difference (t=0.548, P=0.604);in the white matter of spinal cord, the number of KPC2/PCNA co-expression cells was (3.86±0.90)/visual field in the control group and (0.71±0.49)/visual field in the experimental group, showing significant difference (t=7.778, P=0.000). And then, the number of KPC2/PCNA co-expression cells were (0.57±0.53)/visual field in the control group and (5.57±1.13)/visual field in the experimental group, showing significant difference (t=8.101, P=0.000). Concomitantly, there was a similar kinetic in proliferating astrocytes in vitro. The Western blot analysis showed a significant down-regulation of P27kip1 and a concomitant up-regulation of KPC2 and PCNA after serum stimulated. Co-immunoprecipitation demonstrated increased interactions between P27kip1, KPC1, and KPC2 after stimulation. ConclusionThe up-regulated expression of KPC2 after SCI is related to the down-regulation of P27kip1, this event may be involved in the proliferation of astrocytes after SCI.
In order to study the prophylactic and therapeutic effect of methyl-prednisolone (MP) on traction injury of spinal cord, 48 rabbits were divided into four groups randomly. According to decreasing amount of the amplitude of P1-wave, 50% reduction lasted for 5 min and 10 min with MP as experimental group, and 50% 5 min and 10 min with NS as control, the changes of amplitudes were monitored by, and the function of the spinal cord was assessed. The amounts of MDA and SOD of the spinal cord tissue were determined and the pathomorphological changes of the spinal cord were observed. The results showed that in the experimental groups, the recovery of P1-wave was quicker, the Tarlov and Molt value were decreased, the density of gray matter of the anterior horn and the myelinated nerve fiber of white matter of 100 microns diameter were higher, the SOD and MDA was decreased and the degenerative and necrotic degree of neuron and nerve fiber were milder. Where in the control groups all the above items were just on the opposite. The conclusions list as follows: the application of MP before operation of spinal deformity might prevent traction injury of the spinal cord during operative correction of spinal deformity, and could also minimized the secondary damage to spinal cord from traction injury if MP was used in time. The action to MP were summarized as improving the microcirculation, inhibiting the hyperoxidation of lipid and accelerating the recovery of SCEP.
ObjectiveTo analyze the protective mechanism of spinal cord ischemia-reperfusion injury mediated by N-methyl-D-aspartate (NMDA) receptor.MethodsA total of 42 SD rats were randomly assigned to 4 groups: a non-blocking group (n=6), a saline group (n=12), a NMDA receptor blocker K-1024 (25 mg/kg) group (n=12) and a voltage-gated Ca2+ channel blocker nimodipine (0.5 mg/kg) group (n=12). The medications were injected intraperitoneally 30 min before ischemia. The neural function was evaluated. The neuronal histologic change of spinal cord lumbar region, the release of neurotransmitter amino acids and expression of spinal cord neuronal nitric oxide synthase (nNOS) were compared.ResultsAt 8 h after reperfusion, the behavioral score of the K-1024 group was 2.00±0.00 points, which was statistically different from those of the saline group (5.83±0.41 points) and the nimodipine group (5.00±1.00 points, P<0.05). Compared with the saline group and nimodipine group, K-1024 group had more normal motor neurons (P<0.05). There was no significant difference in glutamic acid concentration in each group at 10 min after ischemia (P=0.731). The nNOS protein expression in the K-1024 group was significantly down-regulated compared with the saline group (P<0.01). After 8 h of reperfusion, the expression of nNOS protein in the K-1024 group was significantly up-regulated compared with the saline group (P<0.05).ConclusionK-1024 plays a protective role in spinal cord ischemia by inhibiting NMDA receptor and down-regulating nNOS protein expression; during the reperfusion, K-1024 has a satisfactory protective effect on spinal cord function, structure and biological activity of nerve cells.