摘要
BACKGROUND： Previous studies have shown that direct current electrical fields affect development and growth of human microvascular endothelial cells, but the role of electrical fields on promoting angiogenesis in tissues following spinal cord injury remains poorly understood. OBJECTIVE： To determine the effects of electrical fields on angiogenesis and spinal cord repair following traumatic spinal cord injury in rats. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Chongqing Key Laboratory of Neurology, Affiliated Hospital of Chongqing Medical University, China from September 2007 to August 2008. MATERIALS： Hydrogen blood flow detector （Soochow University Medical Instrument, China）, Power Lab System （AD Instruments, Colorado Springs, CO, USA） and mouse anti-vascular endothelial growth factor （VEGF） monoclonal antibody （Sigma-Aldrich, St. Louis, MO, USA） were used in this study. METHODS： A total of 60 healthy, adult, Sprague Dawley rats were equally and randomly assigned to sham-surgery, model, and electrical field groups. The Allen＇s weight-drop method was used to induce complete spinal cord injury in the model and electrical field groups. Rats in the electrical field group were implanted with silver needles and electrical fields （350 V/m） were applied following traumatic injury. MAIN OUTCOME MEASURES： Latency of somatosensory-evoked potential was detected and spinal cord blood flow was measured by hydrogen blood flow detector. Microvascular density was determined by histological analysis. VEGF expression in the spinal cord was observed by immunohistochemical staining. RESULTS： Recovery of spinal cord blood flow was significantly increased in the electrical field group （at 1, 2, 4, 8, and 24 days after injury） compared with the model group （P 〈 0.05 or P 〈 0.01）. Latency of P1 waves in somatosensory-evoked potential of electrical field group （at 1,2, 4, 8, and 24 days after injury） was significantly shorter than the model group （P 〈 0.05 or P 〈 0.01）. Microvascular density and VEGF expression were greater in the electrical field group compared with the model group at 24 days after injury （P 〈 0.01）. CONCLUSION： Electrical fields （350 V/m） promoted angiogenesis within injured rat tissue following spinal cord injury and improved spinal cord function. Electrical fields could help to ameliorate spinal cord injury. The mechanisms of action could be related to increased VEGF expression.
BACKGROUND： Previous studies have shown that direct current electrical fields affect development and growth of human microvascular endothelial cells, but the role of electrical fields on promoting angiogenesis in tissues following spinal cord injury remains poorly understood. OBJECTIVE： To determine the effects of electrical fields on angiogenesis and spinal cord repair following traumatic spinal cord injury in rats. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Chongqing Key Laboratory of Neurology, Affiliated Hospital of Chongqing Medical University, China from September 2007 to August 2008. MATERIALS： Hydrogen blood flow detector （Soochow University Medical Instrument, China）, Power Lab System （AD Instruments, Colorado Springs, CO, USA） and mouse anti-vascular endothelial growth factor （VEGF） monoclonal antibody （Sigma-Aldrich, St. Louis, MO, USA） were used in this study. METHODS： A total of 60 healthy, adult, Sprague Dawley rats were equally and randomly assigned to sham-surgery, model, and electrical field groups. The Allen＇s weight-drop method was used to induce complete spinal cord injury in the model and electrical field groups. Rats in the electrical field group were implanted with silver needles and electrical fields （350 V/m） were applied following traumatic injury. MAIN OUTCOME MEASURES： Latency of somatosensory-evoked potential was detected and spinal cord blood flow was measured by hydrogen blood flow detector. Microvascular density was determined by histological analysis. VEGF expression in the spinal cord was observed by immunohistochemical staining. RESULTS： Recovery of spinal cord blood flow was significantly increased in the electrical field group （at 1, 2, 4, 8, and 24 days after injury） compared with the model group （P 〈 0.05 or P 〈 0.01）. Latency of P1 waves in somatosensory-evoked potential of electrical field group （at 1,2, 4, 8, and 24 days after injury） was significantly shorter than the model group （P 〈 0.05 or P 〈 0.01）. Microvascular density and VEGF expression were greater in the electrical field group compared with the model group at 24 days after injury （P 〈 0.01）. CONCLUSION： Electrical fields （350 V/m） promoted angiogenesis within injured rat tissue following spinal cord injury and improved spinal cord function. Electrical fields could help to ameliorate spinal cord injury. The mechanisms of action could be related to increased VEGF expression.
基金
the National Natural Science Foundation of China,No.30300075
the Sichuan Science Fund for Outstanding Youths,No.05ZQ026-020
the China Postdoctoral Science Foundation Project,No.20080440996
