Sakai Noriko, Mizuno Risuke, Ono Nobuyuki, Kato Hiroyuki, Ohhashi Toshio
Department of Physiology, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, 390-8621 Japan.
Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1498-507. doi: 10.1152/ajpheart.01190.2006. Epub 2007 May 18.
Microcirculation of the sheath of the rat sciatic nerve fiber was investigated by using an intravital microscope, and changes in the diameter of the epineurial arterioles in response to highly oxygenated Krebs-bicarbonate solution were evaluated. Superfusion of low-oxygen (0%) Krebs-bicarbonate solution (LKS) onto rat sciatic nerves did not affect changes in the diameter of the arterioles. Nifedipine, a Ca(2+)-channel blocker, caused a dose-dependent dilation of the epineurial arterioles in LKS. In contrast, superfusion of high-oxygen (21%) Krebs-bicarbonate solution (HKS) onto rat sciatic nerves significantly constricted the epineurial arterioles in a time-dependent manner. The HKS-induced constriction of the epineurial arterioles was significantly reduced by treatment with 120 U/ml superoxide dismutase (SOD) alone or 5,000 U/ml catalase alone. In the presence of 120 U/ml SOD plus 5,000 U/ml catalase, 10(-4) M tempol, 10(-6) M diphenyleneiodium, 2 x 10(-4) M apocynin, or 10(-6) M allopurinol, the HKS-induced constriction of the epineurial arterioles completely disappeared. These results suggest that superfusion of highly oxygenated solution onto rat sciatic nerves constricts the epineurial arterioles through reactive oxygen species (ROS), including superoxide and hydrogen peroxide, and that production of superoxide involves a NADPH oxidase- or xanthine oxidase-dependent pathway. In conclusion, ROS play significant roles in the regulation of microcirculation of rat sciatic nerves in vivo.
利用活体显微镜研究大鼠坐骨神经纤维鞘的微循环,并评估神经外膜小动脉直径对高氧克雷布斯 - 碳酸氢盐溶液的反应变化。向大鼠坐骨神经灌注低氧(0%)克雷布斯 - 碳酸氢盐溶液(LKS)对小动脉直径变化无影响。钙通道阻滞剂硝苯地平可使LKS中的神经外膜小动脉呈剂量依赖性扩张。相反,向大鼠坐骨神经灌注高氧(21%)克雷布斯 - 碳酸氢盐溶液(HKS)会使神经外膜小动脉随时间显著收缩。单独用120 U/ml超氧化物歧化酶(SOD)或5000 U/ml过氧化氢酶处理可显著减轻HKS诱导的神经外膜小动脉收缩。在存在120 U/ml SOD加5000 U/ml过氧化氢酶、10⁻⁴ M tempol、10⁻⁶ M 二亚苯基碘鎓、2×10⁻⁴ M 阿朴吗啡或10⁻⁶ M 别嘌呤醇的情况下,HKS诱导的神经外膜小动脉收缩完全消失。这些结果表明,向大鼠坐骨神经灌注高氧溶液会通过包括超氧阴离子和过氧化氢在内的活性氧(ROS)使神经外膜小动脉收缩,且超氧阴离子的产生涉及NADPH氧化酶或黄嘌呤氧化酶依赖性途径。总之,ROS在体内大鼠坐骨神经微循环调节中起重要作用。